If disease is altered cell biology, what then are the factors that cause diseases? What are things that can change the cell’s condition? Watch and listen as Leslie discusses the five causes of diseases. Whatever the disease is, they will always be attributed to one of the five causes. Sounds simple, right?

Hope you have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun. My name is Leslie Samuel, and in this video, I’m going to be talking about the five causes of disease.

Last episode, Episode 70, we spoke about what a disease is, and if you watched that video, you’ll know that a disease at some level, is some kind of altered cell biology. So, what we’re talking about now is five causes of altered cell biology. If you need to revisit that episode, just head back over to Episode 70, and you’ll learn about that.

What are the five causes of disease?

Cause number one is adaptation. What we’re saying here is that there’s some kind of an injurious agent that comes into the environment of a cell, and the cell tries to adapt to that agent, and that can cause altered cell biology.

Number one is adaptation. Number two is injury. There is an injurious agent the cell tries to adapt, and it does certain things to try to adapt, and at a certain point, it can no longer adapt, and the cell becomes injured.

Cause number one, adaptation. Cause number two, injury. And, then, if we go one step beyond that, there’s cellular death. So, the cell tries to adapt, it gets injured, and if that injurious agent stays around for long enough, that can cause the cells to die.

So, cause number one, we have adaptation. Cause number two, we have injury. And, cause number three, cellular death. And then, there’s a fourth cause, and this is called neoplasia. And, what this is is when there’s something that causes the cell to uncontrollably divide. In other words, we’re talking here about cancer. So, the fourth cause of altered cell biology is neoplasia.

And then, the last cause, cause number five is aging. The cells get older, and as they get older, certain things happen that cause the cell’s biology to be altered.

So, there we have it, the five causes. Cause number one is, adaptation. Cause number two is injury. Cause number three is cellular death. Cause number four is neoplasia. And, cause number five is aging.

I don’t care what disease you’re talking about, but we can fit all of them into one or more of these five causes.

That’s it for this video. My name is Leslie Samuel from Interactive-biology.com. I want to invite you to go back to the website, and check out other videos that we have, and other resources to help make Biology fun.

That’s it for this video, and I’ll see you on the next one.

This is the first in Leslie’s joke series. Something for your amusement and pleasure. It’s time to get some time off from all the books and give yourself a little laughter.

Listen to the story of the intelligent professor as he collects his observation about his frog experiment. Would you have thought about it this way too?

As promised, here is the start of a set of new videos to be uploaded to the site. Let’s start off this year by learning what a disease is from a Biological perspective.

Also, you’ll notice something new with the video format. Let me know what you think.

Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 070, I’m going to be answering a simple question, What is a disease? I know what you’re thinking. Everybody knows what a disease is. But, since this Interactive Biology, we’re going to look at it from a Biological perspective. So, let’s get right into it.

A disease is an abnormal condition that affects the body of an organism.

What’s an organism? An organism is a living thing. And, when we’re talking about Pathology, or Pathophysiology, we’re talking about human beings. So, we’re talking about an abnormal condition that affects the body of a human being. A disease is usually associated with a number of symptoms or signs. But, what does these all really means?

Okay, so we have an abnormal condition affecting the body. But, what is the body? I know what you’re thinking, the body of a human being is made up of systems. So, we have the circulatory system, we have the muscular system, the skeletal system, the urinary system, all of these different systems that come together to form a human being.

But, what are these systems? I know what you’re thinking now. You’re thinking these systems are made up of organs, and you’re right! For example, the circulatory system is made of the heart, and the blood vessels and all these things come together to form the circulatory system.

But, what is an organ? I know what you’re thinking because you’re smart. An organ is made up of tissues. All right, so we have it down to the tissue level. But, what is a tissue? Finally, you’re there. A tissue is made up of cells. All living things — human, or dog, or cat, or wolf, whatever it is, all living things are made up of cells.

So, if you have an abnormal condition that affects an organism, that’s because we have something that’s affecting one or more of the organ systems. And then, of course, it’s affecting one or more of the organs, one or more of the tissues, and one or more of the different cell types. So, in essence, what we’re saying is, if we have a disease, we have an abnormal cellular structure, and/or function, there is something wrong at the cellular level that’s causing this thing to be manifested on the level of the organism.

Now, there are many different types of diseases. But, I’m going to tell you something that’s going to make it much more simple. All of these disease can be attributed to one of five causes. Doesn’t that sound simple? If we know these five causes, we could explain to some level every single disease that’s out there.

What are those five causes? That’s what we’re going to talk about in the next episode.

That’s all for this episode. Once again, I want to invite you to come back to the website at Interactive-biology.com, where you’re going to find more videos just like this, and many other resources to help you make Biology fun.

By the way, what do you think about this new video format? Let me know in the comments below. That’s it for now, and I’ll see you in the next video.

Interactive Biology by Leslie Samuel is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.

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The central nervous system is such a delicate part of our body that it needs a stable protection against damage and injuries. Learn what protects and surrounds it from the pressures outside of the body.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel, and in this episode, Episode 069, I’m going to be talking about the meninges of the Central Nervous System. So, let’s get right into it.

Now, the central nervous system is very delicate and needs to be protected. Speaking about delicate central nervous systems, over here to the right we have an interesting picture. This picture basically shows archaeological remains of patients of brain surgery, and they were performed by the ancient doctors of the Incan empire back in the 15th century. You can see we have some significant holes here.

In studying these archaeological remains, we are able to see that significant advances were made to where the success rate of the doctors and the surgeons that performed these surgeries was up to 90 percent. So, there’s a lot going on there, but that’s not the topic for this episode. We’re going to talk more about the meninges as opposed to the archaeological stuff.

Part of the protection is provided by the meninges. We need to protect the brain, we need to protect the spinal cord, and part of that protection is done by the meninges.

The meninges surround the central nervous system, so they go around the central nervous system, and they suspend it in a protective jacket. That protective jacket is filled with CSF. That stands for ‘cerebrospinal fluid.’

Let’s kind of try to visualize this. Here we have a picture. This is showing the brain. This part here is the brain, so this is dealing with the cortex. As you can see, we have a number of layers even before we get to the bone.

The first layer is called the, ‘pia mater,’ and then, we have the ‘arachnoid layer,’ and ‘dura mater.’ So, pia mater, arachnoid, and dura mater. A good way of remembering this from inside to out is, you have a P.A.D. that surrounds your brain: ‘P’ for pia mater; ‘A’ for arachnoid, and ‘D’ for the dura mater. And then, of course, we have the bone, the periosteum, which is the membrane that surrounds the bone, and then, we have the skin.

The three meninges– pia mater, arachnoid, and dura mater, and you can also see that over here. Here, we’re looking at the brain. So, this is the cerebrum. You can see, we have this very thin layer that’s directly connected to the brain. That is the pia mater, then, we have a space. This is called , the ‘subarachnoid space,’ but, we’re not going to go into that in this video.

Then, we have this green line that goes around here, and that thin line is the arachnoid. And then, we have a thicker band, and that is the dura mater. That’s the wider part here. So, those are the three layers, .A.D.

Let’s look at a different picture that shows the same thing here. We have this red line as the pia mater. And then, we have this space, then, we have this thin line here. That is the arachnoid, and we have the dura mater. Pia, arachnoid, and the dura.

As you can see, the dura is the thickest, then we have the arachnoid, and then, the very thin pia mater.

All right, so, if you want to look at an organizational chart, here we have the meninges, and the three types are the dura mater, arachnoid mater, and pia mater—those are the three meninges. And then, we can take the dura mater and subdivide that into the meningeal layer and the peritoneal layer.

The peritoneal layer is the layer that is attached to the bone. So, the dura mater has two layers: The meningeal layer and the peritoneal layer.

The arachnoid and pia mater, those are thin layers that we can put together and call leptomeninges. “Lepto” comes from the Greek word that means “thin or fine,” and “dura ” means tough. And, that’s why you get words like , “Durable.” Something that’s durable is very tough. The dura mater is tougher, and it’s stronger and thicker, and then, we have the two thin layers called the arachnoid and pia mater. Both of them, we can take them together and call them, ‘leptomeninges.’

That’s all I want to talk about in this video. As usual, I want to invite you to visit the website, Interactive-Biology.com for more Biology videos, other resources… We just released a new Interactive study Guide, and you can check that out. You can get all the resources at the site, to help make Biology fun.

This is Leslie Samuel. That’s it for this video, and I’ll see you in the next one.

In this episode, Leslie talks about our “little brain,” or our cerebellum — about its different parts and functions of each. The cerebellum has three fiber peduncles attaching it to the brain stem, and also has three lobes just like our brain. Learn more about the functions and locations of each as you watch through this episode.

Enjoy!

Also, check out the following video about a boy that was born without a Cerebellum. It will give you a better understanding of what the Cerebellum does.

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel, and in this episode, Episode 068, I’m going to be talking about the anatomy and functions of the cerebellum. So, let’s get right into it.

Here, we’re looking at a picture of the cerebellum. The cerebellum would be this part here, then, of course, we have the brain stem that is just anterior to the cerebellum. Of course, superior to that we have the cerebrum. This is just looking at a section of the brain, the section showing the cerebellum. Just to let you know, if you want to revisit what I’ve already said about the cerebellum, you can go to Episode 026. In Episode 026, I talk about the functions of the cerebellum, and I go into a little bit of detail.

What we’re going to do is we’re going to build on what we spoke about in that episode and talk a little more about the anatomy and the functions of the cerebellum.

Just to recap, “cerebellum” is Latin for “little brain.” It looks like a little brain at the back and the bottom of the brain. So, posterior and inferior, that would be where the cerebellum is located. The functions of the cerebellum, of course, we’re dealing with integration, regulation, and coordination of motion.

You want to move from one location to the next, you want to move your arm, you want to move some part of your body, the cerebellum is very much involved in integrating the signals or regulating what’s going on and coordinating that motion. That is the cerebellum and what it does.

Here’s a different picture of the cerebellum. You can see, we have the cerebellum here. It’s a drawing of the cerebellum from Gray’s Anatomy. Here you can see we have the brain stem. Of course, at the top, we’re going to have the midbrain, and then the pons, and the medulla.

What I want to emphasize here is that we have three pairs of fiber bundles that are attaching the cerebellum to the brain stem. Those fibers are called the cerebellar peduncles. We have three pairs of them. You can see here, we have the superior peduncle. (This is pointing out one of the superior peduncles). Then, we have, of course, the middle peduncles (so, that would be those fibers here). And then, we have the inferior peduncles which would be, of course, beneath the middle peduncles. You can see one here, and one over here.

We have these three pairs of peduncles, the superior peduncles, middle peduncles, and the inferior peduncles. Those connect that cerebellum to the brain stem. Of course, they’re going to connect to different regions. The superior peduncles are going to connect to the upper pons, (so, here we have the pons, and that’s connecting to the upper pons). The middle peduncles are going to connect it to the lateral aspect of the pons, (that’s right here). And then, the inferior peduncles, it’s going to connect to the dorsal lateral surface of the upper medulla. So, here we have the medulla, dorsal, that would be kind of to the back here; and lateral, so, we’re dealing with the upper medulla in this area. That’s where the inferior peduncles connect. We have all these fibers that are connecting the cerebellum to the brain stem.

Let’s move on from there and take at another look at the cerebellum. What we’re doing here, in these pictures, these are pictures of a cerebellum from a human, but in the top picture, we are looking at the posterior view, so from the back of the head, here, we are looking at the anterior view. This is the side of the brain stem. The brain stem would normally be in the front here. So, posterior and anterior.

What I want to show you is that we have three lobes in the cerebellum. Just like the brain has lobes, cerebellum is a little brain. It also has its lobes. Those three lobes are the anterior lobe, which of course, would be the one that you’re seeing here. So, these would be the two anterior lobes. Then, if you look from the back, you get the posterior lobe, so you can see this is one posterior lobe, and this is another posterior lobe.

Then, we have the flocculonodular lobe. That would be inferior, but it’s kind of small, so you can’t see it, as well, (it’s not shown in this picture). It’s kind of blocked by the posterior lobe. So, we have the anterior lobe, posterior lobe, and the flocculonodular lobe. Those are the three lobes.

The largest lobe would be, you can see that here, the posterior lobes. You can see that’s bigger than the anterior. The smallest would be the flocculonodular lobe.

There’s one more structure that I want to talk about. That is called the vermis. You can see the vermis right there, kind of in between the two lobes.

The cerebellum is involved in integrating, regulating, and coordinating motion. It needs to get input from the regions of the brain that are responsible and that are involved in that process. It needs to get information from the different parts of the central nervous system. These three lobes are going to get information from different parts. And, the anterior lobe gets information from the spinal cord. So, you have these peripheral nerves coming into the spinal cord giving information about what’s going on in the periphery of your body, what’s going on with your hands, and your legs, your extremities. It’s going to take that information, of course, and integrate that with some other information that the cerebellum is getting.

The posterior lobe is going to get information from the cortex. We’ve spoken about areas in the cortex. We’ve spoken about areas in the cortex that are responsible and that are involved in the process of movement.

And, lastly, the flocculonodular lobe is going to get information from the vestibuli. That’s in the inner ear. The vestibuli are heavily involved in proprioception being aware of where your body is.

So, anterior lobe getting information from the spinal cord; the posterior lobe getting information from the cortex; the flocculonodular lobe getting information from the vestibuli. The cerebellum is taking all that information, processing it, and helping you to have coordinated motion.

I hope that makes sense. That’s pretty much all I want to cover in this episode. As usual, I want to invite you to visit the website at www.Interactive-Biology.com. You’re going to get more Biology videos there, more resources to help make Biology fun, transcripts of these videos and just a bunch of other stuff. So, head on over there, www.Interactive-Biology.com.

This is Leslie Samuel. That’s it for this video, and I’ll see you on the next one.

Leslie is on a roll today! In this next episode, he tackles about the parts and functions of the occipital and temporal lobes: the occipital lobe being the primary visual cortex and the temporal lobe being involved in processing auditory signals. Watch to learn more about these parts of the brain and their functions, as well.

Have fun!

Transcript of Today’s Episode

Hello and welcome to another of episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel, and in this episode, Episode 067, I’m going to be talking about the anatomy and functions of the occipital and temporal Lobes. Let’s get right into it.

The occipital lobe, you can see it here, to the posterior end of the brain, and it’s here in pink. You just see a small surface here, but I do want to emphasize that it also extends medially. It’s more prominent as you go medially into the brain. We’re going to see that in the next slide.

This is the primary visual cortex. When you see something, light is coming into the eyes. It’s hitting the rods and the cones in the retina, and there are some signals being sent to the brain. Those signals that are sent to the brain are coming to the visual cortex in the occipital lobe, and then, there’s processing that’s happening there.

If you want to review how that happens in the eyes, you can check out Episode 034 and 035 where we deal with some of those things in terms of how the rods and the cones process the information, and then, how they are sent to the brain. This is the region in the brain that they’re coming so that they can be processed, and so that you can see this screen and you can see all of the things that you see.

Let’s look at a mid-sagittal section, so that we can see the medial aspect of the brain, and you can see here (let’s do it in blue), you can see in this area, we have the occipital lobe. You are just seeing the outside surface and it does extend more medially. You can see that here.

Okay, so let’s move on now to the temporal lobe. The temporal lobe, you can see, is over here. It’s kind of to the side of the brain, and it’s in green. And, the temporal lobe is involved in processing auditory signals.

We’ve spoken about how hearing happens. You can look from Episode 036 through 040. I covered hearing there. Specifically, in Episode 040, I spoke about the hair cells, and about how when you hear something, there are vibrations that are happening. That causes the hair cells to bend, and when they bend, they send signals to the brain. This is the region we’re talking about in the brain.

Now, specifically, there’s a region that’s not shown, the Gyri of Heschl, and that is found in the most superior inner aspect of the temporal lobe. As we go more medial, you will see, we have some gyri, and we call those Gyri of Heschl, and that is where we find the primary auditory receiving area. This is where the signals are coming from the hair cells, so that we can hear stuff.

All right. Let’s go a little further into the temporal lobe. We’re going to look at the three regions. We have the superior temporal gyrus, the middle temporal gyrus, and the inferior temporal gyrus. Those are the three sections. And you can see they’re separated by these two sulci.

When I look at something that’s moving, there’s some processing that needs to happen for me to understand that that object is moving. And there are regions in the middle and inferior Gyri that are involved in perceiving moving objects, and also recognizing faces. So, you’re getting now into some more detailed processing so that you can see someone and recognize who they are by looking at their face. You can understand that objects are moving because of the processing that’s happening in these areas.

That’s pretty much all I want to say about that for now. As usual, you can visit the website at www.Interactive-Biology.com, and there you can find more Biology videos. You can find transcripts of all the videos so you can print them out and read them. You can find all kinds of resources to help make Biology fun.

This is Leslie Samuel. That’s it for now, and I’ll see you in the next one.

Today, Leslie discusses the parts and functions of the parietal lobe. Among it’s parts, Wernicke’s area is said to help us understand spoken language. The parietal lobe is also involved in other processes such as perceiving and processing somatosensory events. Watch the video to learn more in detail as Leslie talks about the anatomy and functions of this part of the brain.

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 066, I am going to be talking about the anatomy and functions of the parietal lobe. So, let’s get right into it.

The parietal lobe, as you can see here, is this region right here. We’re starting at the central sulcus, it goes down, and on the inferior end over here, we have the lateral cerebral fissure, and posteriorly, we have the parietal occipital fissure that separates the parietal lobe from the occipital lobe.

The parietal lobe is primarily involved in perceiving and processing somatosensory events. We’re talking about things like touch, and temperature, and body position, and pain. The term that we use for body position is proprioception, and the term that we use for pain is nociception. So, proprioception and nociception, those are also involved in the processing of the parietal lobe. Let’s go a little more into that.

Here we have, on the most anterior end, we have the postcentral gyrus. Of course, the postcentral gyrus is going to be just posterior to the central sulcus. And then, we have the postcentral sulcus on the posterior end of that gyrus. The function of that gyrus is basically receiving somesthetic information. We’re talking about kinesthetic and tactile information. “Kinesthetic,” meaning body movements and “tactile” would be touch. That information comes in and it goes to the postcentral gyrus. There’s some processing that happens there for us to be able to recognize movements of body, and when we get touched we can feel that because of some of the processing that’s happening right here.

Of course, the left half of the brain, so the left postcentral gyrus is going to be getting information from the right side of the body, and the right postcentral gyrus is going to be receiving information from the left side of the body. Not only that, but it’s also what we call somatotopically organized. What that means is specific parts of the postcentral gyrus are going to receive information from specific parts of the body.

For example, if we are looking at the face and head, the information that’s coming from the face and the head are going to be processed in the most inferior parts of the postcentral gyrus. As we go more superior, we’re going to be starting to get input from the upper limbs. If we go more medial, we’re going more towards the center of the brain, we’re going to be getting information from the lower limbs.

So, it’s somatotopically organized, specific parts of this gyrus gets information from specific parts of the body. We’re going to see that a lot in the different parts of the brain. So, postcentral gyrus, we spoke about that.

Then, we have the superior parietal lobule, and of course, that’s going to be superior. What that does is it integrates sensory and motor functions. Then, we have the inferior parietal lobule. You can see that the superior and inferior parietal lobules are separated by this intraparietal sulcus. “Intraparietal,” “intra” means it’s inside, or in between. “Parietal,” the parietal lobe. That’s the intraparietal sulcus.

In the inferior parietal lobule, you see here we have the supramarginal gyrus and the angular gyrus. These two gyri receive input from the auditory and visual cortices, and of course, it’s processing auditory information and visual information. In order for us to see and hear, we’re getting information through this supramarginal gyrus and the angular gyrus.

Then, we have a specialized area that’s called Wernicke’s area. I know it looks different than I’m pronouncing it, but that’s the German pronunciation. What that helps us do is understand spoken language. So, someone is speaking to you, and you need to understand what they are saying. There’s processing that’s happening in the Wernicke’s area. Of course, in some cases, it’s more difficult to understand some people than others. (I’m sorry I shouldn’t have done that).

Okay, let’s continue. If there’s damage to this area, so if we have like lesions in the Wernicke’s area, that can result in Wernicke’s aphasia. What that is, is impairment of comprehension and repetition. You have a hard time understanding spoken language because of the damage in this area.

That’s pretty much it. That’s all I want to cover for this episode. As usual, I want to invite you to visit the website at www.Interactive-Biology.com for more Biology videos. You can also get the transcripts of every video that I have posted here, all of the Interactive-Biology TV videos, and a bunch of other resources to help make Biology fun.

That’s pretty much it for now, and I’ll see you on the next one.

Learn more about the brain gyri and sulci or fissures. Get familiar with the anatomy and functions of the frontal lobe in this easy to understand video. Leslie has also included an interesting video about an individual with Broca’s aphasia, a defect in the Broca’s Motor Speech area resulting in speech problems.

Have fun learning!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 065, I’m going to be talking about the anatomy and functions of the frontal lobe. But, before I talk about that, let’s talk about the folds in the cerebrum.

Now, when we’re talking about ‘gyri,’ we’re talking about the folds. You can see here in this brain, we have all these little folds that go all throughout the brain. Those are called ‘gyri.’ If you’re dealing with one of them, you’re not going to say gyri, but you’re going to say ‘gyrus.’

Then, we have the ‘sulci’ or the ‘fissures.’ Sometimes, we use these interchangeably, but these are the depressions in the brain that define the lobar boundaries. Here, we have the different lobes, and you can see we have all of these depressions, in other words, we have all of these grooves that are going throughout the different lobes of the brain. Those are called, ‘sulci,’ and in some cases, we call them, fissures.

So, with that understanding, let’s look at the frontal lobe in the brain. Now, the frontal lobe, we have two major boundaries that define the frontal lobe. Over here, we have the central sulcus. You can see that’s going through here. That is the posterior aspect (okay, so that’s towards the back). The posterior aspect of the frontal lobe, the boundary is the central sulcus.

Then, if we go inferiorly here, we have the lateral sulcus, or we can call it the Sylvian sulcus. That’s this boundary here on the inferior end of the frontal lobe. The central sulcus, posteriorly, and the Sylvian or lateral sulcus, inferiorly. And, this here would be the frontal lobe.

The first thing I want to talk about is this section here that’s called the precentral gyrus. Here, you can see in this case, it’s called the anterior central gyrus, but this is the precentral gyrus. The function of that region is it serves as the primary motor cortex. So, it’s basically getting motor signals from different parts of the brain, and it’s integrating it in this region. The precentral gyrus. This is where a lot of that motor function is integrated.

Just anterior to that, it’s not shown in this image, but I’m just going to kind of draw a section in here coming from the, from this part all the way. Maybe it’s not that right. It’s kind of, it’s not exact, but this is the pre-motor cortex, which makes sense. If this is the primary motor cortex, and this is, right before that, it’s the pre-motor cortex. Here, we have kind of an area that we call the ‘supplemental motor area.’ So, it’s the supplemental motor area. That plays a big role in initiating movements. You want to move, there’s an initiation that has to happen, and this has something to do with that process of initiating movements.

Now, as I said before, the boundaries aren’t necessarily definitely defined. I can’t see that it goes from right here to right there. But, in this area here, let’s show this area. I’ll just color it in a little bit. We have what’s called the ‘frontal eye fields.’ (Let me write that out—frontal eye fields). And, that is involved in the movement of the eyes, but a specific movement. When I look to the left and I look to the right, my eyes are moving horizontally. The frontal eye fields are involved in the horizontal movement of the eye.

Let’s move on. Then, we have, if we go anterior from that area, we have the superior frontal gyrus, the middle frontal gyrus, and the inferior frontal gyrus. So, superior, middle, and inferior frontal gyrus.

And, in the left hemisphere of the brain in the frontal lobe, we have an area that we call the Broca’s motor speech area. That has a big part to do with the motor components of speech. So, you’re speaking, I am speaking into this microphone right now, my mouth is moving in certain ways, and there are muscles that are controlling that, and this Broca’s motor speech area is very much involved in that process. Once again, it’s in the left hemisphere, not the right, and that deals with motor control of speech.

Now, if there’s damage to this area. If something happens, and that causes this area to be damaged, the result of that can be what we call, ‘Broca’s aphasia.’ When you have that condition, it causes a form of language impairment where you cannot speak well. It’s not that you can’t comprehend, but the motor control of that speech doesn’t function as well because the Broca’s motor speech area is damaged.

I have a little video here to show an example of that. So, let’s go ahead and take a look at that right now. (Video starts to play).

So, this is an example of Broca’s aphasia. You can see he had some problems speaking. Not necessarily in comprehension, but in just the motor control in forming the words and putting together long strings of the words to make complete sentences. That is an example of Broca’s aphasia.

If we look all the way into the anterior section, you’ll see that we have the prefrontal cortex and that plays a very important role in the process of intellectual functioning, and emotional responses, and so on. So, intellectual and emotional events that has a lot to do with what happens in the prefrontal cortex.

There’s another area that we cannot see in this picture, and in order to see it, we need to remove a section from here because it’s deeper in, it’s more medial. We’re going to do that now, and take a look at that. Here, you can see we have removed the part of the temporal lobe and part of the frontal lobe and then, here, there’s an area that we call the ‘insula.’ You can see it over here, and you can also see right here. This is the insular cortex. This picture over here is a coronal section of the brain. We just take a section of the brain right in this area, and you can see the insula right here.

Depending on what book you read, you might get different explanations as to the function of the insula, anything from taste, sensation, to emotions, to thoughts, pain sensations, visual sensations in terms of, you know, feeling hungry and thirsty. That’s attributed to that region. We’re not 100% clear on how this works, but we do have some suggestions as to its function.

The last thing I want to talk about is what we see right here. This structure is called the corpus callosum. That is responsible for connecting the two hemispheres, and you can see as the cortex goes medially, it borders in the inferior aspect with that corpus callosum. We can see it even clearer here. We can see the corpus callosum. You can see it starts here in the frontal cortex, and it goes back here. So, this is the corpus callosum. If we’re dealing with the frontal cortex, that does border with the corpus callosum inferiorly. That is shown very well right there.

That’s pretty much all I want to cover for this episode. As usual, you can visit the website at Interactive-Biology.com for more Biology videos. You could find transcripts of all the videos and a number of other resources to help make Biology fun.

This is Leslie Samuel. That’s it for now, and I’ll see you in the next one.

http://www.youtube.com/watch?v=vhBRo1cMocA

Here’s another whole new episode to make anatomy easier for everyone. Learn about the different anatomical planes with Leslie as he goes through each one including the spatial relationships between parts in the human body. This will be a great help when you go deeper into anatomy and neuroanatomy making it easier for everyone to understand and learn new concepts.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel. In this episode, Episode 064, I’m going to be talking about the anatomical planes and spatial relationships in the human body. As we go into neuroanatomy, we’re going to need to know these planes and these spatial relationships. Let’s get right into it.

Here we have the human body. I want to talk about the three different types of planes that we have. First, we have the coronal or the frontal plane. That’s a vertical plane at a right angle to the cerebral axis. You can see that plane here.

If you got a right angle to that, of course, we have the sagittal plane, which is a vertical plane, but it is parallel to the cerebral axis. You can see that plane over here.

We have a mid-sagittal plane, which means it goes through the midline. You can see that plane over here in red, and then, we have a parasagittal plane, which is just off the midline. So, for example, a parasagittal plane would go through, instead of the midline, let’s say, it goes through right about here. And, that continues down just like the mid-sagittal plane. But, instead of going through the midline, it’s just off the midline. That’s parasagittal.

Then, we have the horizontal plane or the transverse plane, which is parallel to the floor.

Let’s look at some location terms in terms of spatial relationships between two parts of the body.
If we’re talking about something that’s ‘superior,’ that means it’s above another part. If it’s ‘inferior,’ which would be the exact opposite, that means it’s below another part. And then, we have terms like ‘rostral,’ which means towards the head. And, this is when we’re looking at general anatomy assuming that we’re talking about beneath the brain, beneath the head. ‘Rostral’ is towards the head, and ‘caudal’ would be toward the tail or the coccyx. In other words it’s the opposite of rostral.

And then, we have ‘anterior,’ that’s towards the front, or ventral, is also towards the front. And then, we have posterior or dorsal, and that’s towards the back. Anterior and posterior are opposite. Dorsal and ventral are opposite terms also.

We have a few more to go over. That would be ‘medial,’ which is towards the midline; ‘lateral,’ which is farther away from the midline as you can see here. We have ‘proximal,’ which is nearest to the point of origin so, it’s closer to something; and ‘distal’ means farther from the point of origin. So, it’s farther away from whatever that point of origin is. That’s not illustrated in the picture over here, but I’m sure you get the point.

Then, we have ‘ipsilateral,’ which is on the same side of the body. Opposite of that would be ‘contralateral,’ which is on the opposite side of the body. For example, if we are looking at the right leg, the ipsilateral arm would be the right arm. The contralateral arm, of course, would be the left arm. So, ipsilateral means it’s on the same side. Contralateral means it’s on the opposite side of the body.

The interesting thing about these directions is what happens when the spinal cord enters the cranium and we get the brain. Because beneath the brain or beneath the head, we said that rostral was towards the head, and caudal was away from the head; ventral or anterior is the front of the body; dorsal or posterior is towards the back of the body.

When we get into the brain, and we pass the midbrain region, which is this region over here, what happens is that there’s a hundred, approximately a hundred-degree bend. So, in other words, it comes and it bends in that direction. What we have then, is dorsal being the top of the brain, and ventral being towards the bottom of the brain; rostral being towards the front, rostral or anterior; caudal being towards the back, or posterior being towards the back of the brain. You can see we have this shift. Instead of dorsal and ventral being towards the back and towards the front. When we’re beneath the brain, as we pass the midbrain region, dorsal now shifts to the top of the brain, and ventral towards the bottom of the brain. So, the ventral surface of the brain would be this surface here. The dorsal surface of the brain would be towards this surface. Caudal surface or the posterior surface of the brain would be this end. And, the rostral or the anterior surface of the brain would be towards this part here.

Another way of looking at this is by looking at these little diagrams over here where we have rostral, caudal, ventral, and dorsal, but when we get above the brain, it’s a little different. It shifts. Rostral is no longer going towards the top, but now, that’s going towards the front. Caudal towards the back. Dorsal towards the top, and ventral towards the bottom of the brain.

However, when it comes to superior and inferior, that stays the same. Superior means towards the top of the brain. Inferior means towards the tail or coccyx, in other words, going towards the bottom. Anterior is always front, and posterior is behind.

This is going to be important when we go into specific details inside the brain and the spatial relationships between the different parts.

That’s pretty much all for now. As usual, I want to invite you to visit www.Interactive-Biology.com, that’s the website where you can find more of these Biology videos, other resources, and a bunch of stuff to help make Biology fun.

This is Leslie Samuel. That’s it for this video, and I’ll see you in the next one.

http://www.youtube.com/watch?v=dOYOdJG0E0s

Join Leslie as he gives you a review of the brain and it’s different major divisions.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV, where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 063, we’re going to take a step back, and we’re going to talk about the divisions of the Nervous System. Let’s get right into it.

If you go all the way back to Episode 001, we spoke about the Nervous System. We said that the nervous system is basically the ‘control center’ of the body.

What we’re going to do is we’re going to take this, and we’re going to look at the divisions within the nervous system. First, we have the Central Nervous System, and we have the Peripheral Nervous System. These are the two systems that we can divide the nervous system into.

The Central Nervous System, that is the processing center of the nervous system. A lot of processing happens here. The Peripheral Nervous System is what connects the Central Nervous System to the limbs and the organs. So, we have the processing in the central, and then, we have the Peripheral Nervous System. These work together very well.

Now, let’s take the Central Nervous System and divide that. That can be divided into the brain and the spinal cord. The brain, that’s center of the nervous system. This is where most of the processing are happening. This is the part that’s found within the skull. This is where things like thought, and emotion, coordinating the body’s activities, all of that stuff happens in the brain.

Then, of course, we have the spinal cord. The spinal cord sends signal to and from the brain, to and from the rest of the body. So, it’s connecting the brain to the rest of the body, basically. Sensory signals come in to the spinal cord, and motor signals go out from the spinal cord. We’re going to talk about those as we deal with the peripheral nervous system. Let’s head on over there right now.

The peripheral nervous, once again, consists of two parts: that’s the Somatic Nervous System and the Autonomic Nervous System.

Let’s talk about the ‘somatic’ first. The Somatic Nervous System is where we’re going to get control of voluntary activities. This is where skeletal muscles are involved. If, for example, I want to walk. I need to contract the muscles in my legs. That is voluntary activity that is controlled by the somatic nervous system. If I want to smile and you can control the muscles in my face. By the way, it takes less muscles to smile than to frown. But, I’m sure you know that. This is all in the Somatic Nervous System.

And, then of course, we have the Autonomic Nervous System which is not voluntary. This is the involuntary things that happen in the body. So, it controls visual functions like heart rate, respiration rate, digestion, those things you don’t need to think about. They just happen. They are “involuntary,” and that is under the control of the Autonomic Nervous System.

We can take the Autonomic Nervous System, and of course, we’re going to divide that into two parts. We have the Sympathetic Nervous System and the Parasympathetic Nervous System.

The Sympathetic Nervous System, that is involved in the ‘flight or fight response.’ It’s what happens to your body when your body is under stress. Things like increasing your heart rate and respiration rate… Anything that you’re increasing. This is usually under the control of the sympathetic nervous system. So, if you go for a nice long jog, and you’re heart rate starts increasing and your respiration rate increases, that is under the control of your sympathetic nervous system.

Then, of course, we have the parasympathetic, which is opposite to the sympathetic. This is involved during rest and digest activities. It’s the opposite of under stress. It’s when there is rest. You’re slowing things down. You’re relaxing. That is more parasympathetic. These are both under the autonomic nervous system.

So, there we have it. Those are the divisions of the nervous system. I hope that was clear to you. That’s pretty much all I want to cover in this video. As usual, I want to invite you to visit the website. You know it. It’s at www.Interactive-Biology.com. There, you can get other Biology videos, and resources to help make Biology fun. This is Leslie Samuel, and I’ll see you in the next one.

http://www.youtube.com/watch?v=eQRODiedQhQ

A lot has happened over the last few months, so go ahead, watch the video, and then let me know what you think in the comments below.

Breathing is one of the most common things we do everyday to a point that it becomes unnoticed. Wouldn’t it be great to learn what happens behind this process? What exactly happens when we breathe air in and out of our body? Watch this video as Leslie teaches once again in such an easy way to make it all easy for us to understand this concept.

Have fun!

Transcript of Todays Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel. In this episode, Episode 62, I’m going to be talking about pressure changes that happen during breathing. That’s what we’re going to talk about. Let’s just get right into it.

We’ve been talking about the respiratory system. We have been talking about the fact that you are breathing in. As air comes in, so let’s say the air is coming through here and then, it eventually ends up in the lungs. In the lungs, we can see here we have the alveoli. As the air comes in, that air can then give oxygen to the blood and it can take carbon dioxide and bring that into the cavity here and then, when you breathe out, of course, that air is going to go through the mouth and through the nose, depending on how you’re breathing and that’s going to push the air outside.

What we’re going to talk about is how this process of breathing actually happens and the pressure changes that are involved.

Here we have the two lungs. What I’m going to do is I’m going to draw an additional part here because this diagram is kind of simplified so, we’re just going to add a little more. We’re going to close this off and we are going to close that part off. And then, I’m going to give some names.

This entire section that we’re dealing with, that is called the thoracic cavity. In the thoracic cavity, we have this space right here. That space is called the pleural cavity. Then, we have one more cavity and that’s inside the lungs. We’re going to call that the pulmonary cavity. Another thing that we need to label here, this here is a muscle and that muscle we call the diaphragm. Beneath here we have the abdominal cavity but, we’re not going to talk too much about that. Actually, let me still label it here because we are going to mention it. Abdominal cavity.

What we’re going to talk about is what happens during breathing. Over here we’re looking at muscles and here you can see we have this group of muscles here and that is called the external intercostals. You can see it diagonally going here. Then, here we have the internal intercostals muscles. So, we’re going to talk about the things that happen during breathing and we’re going to mention what roles those play also.

When I’m breathing in, I’m taking a breath. I just breathe in. There are a number of things that are happening.

First thing is we have the diaphragm here and the diaphragm contracts. When the diaphragm contracts, that moves down. It kind of moves down here. Then, we have the external intercostals. When they contract, that moves the rib cage up. So the diaphragm is contracting; the external intercostals are contracting; this moves down, the external intercostals move the rib cage up and the overall effect is that we’re increasing the space of the thoracic cavity. So, we’re increasing the size of the thoracic cavity. When you increase the size, that is going to cause a decrease in pressure in the thoracic cavity. Of course, since you’re increasing the size and you’re pushing down here with the diaphragm, it’s increasing the pressure in the abdominal cavity, decreasing the pressure in the thoracic cavity. Of course then, that’s going to cause a reduction in pressure of the pleural cavity. When the pressure is reduced in the pleural cavity, that then becomes lower than the pressure inside the lungs in the pulmonary cavity.

Once again, diaphragm contracts, external intercostals contract. That expands the thoracic cavity, decreasing the pressure in the pleural cavity. If we have a lower pressure in here than in the lungs, what is going to happen to the lungs? Of course, greater pressure inside, lower pressure on the outside, the lungs are going to expand. As the lungs expand, now you have more space in here, that’s going to decrease the pressure in the pulmonary cavity, relative to the pressure of the atmosphere. That is going to cause air to move from higher pressure to lower pressure and the air is going to go in and, of course, go into the lungs.

Let’s review that again: Diaphragm contracts, external intercostals contract that expands the thoracic cavity, decreasing the pressure in the pleural cavity. Because that’s going to be now lower than the pulmonary cavity, that’s going to cause the lungs to expand causing a reduction in pressure in the pulmonary cavity. That’s going to cause air to move from the atmosphere into the lungs. And, we have just accomplished breathing in.

During normal breathing, what then happens when it’s time to, not inspire, but expire, so, exhale. The diaphragm and the external intercostal muscles are going to relax. Since we had a buildup in pressure here, when the diaphragm contracted, the abdominal cavity is then going to push against the thoracic cavity increasing the pressure in the pleural cavity, increasing the pressure in the pulmonary cavity causing air to leave. So, it’s the exact opposite.

First, we’re decreasing the pressure by expanding then, now we are increasing the pressure by making the cavity smaller, pushing the air out. That’s during normal breathing.

When you are breathing more intense and it’s more of a forced breathing situation, it’s very similar to what we just described except that there are other muscles involved. So, for inspiration, the diaphragm is going to contract, external intercostals are going to contract and also some neck muscles and we’re going to get air coming in. It’s a stronger contraction. So, that’s going to bring more air in because you’re reducing the pressure even more.

Then, when you’re breathing out, you’re not just relaxing the diaphragm but you’re also bringing in the internal intercostals muscles and those are going to contract and when those contract, the rib cage moves down, thoracic cavity gets smaller, faster of course, and that’s going to increase pressure faster, and cause more air to be pushed out into the atmosphere.

Overall, you’re breathing in because you’re decreasing the pressure on the inside, you’re breathing out because you’re increasing the pressure on the inside.

That’s pretty much all for this episode. As usual, if you want to find more of these videos and other resources I’d like to invite you to visit the website at Interactive-Biology.com. That’s it for this video and I’ll see you on the next one.

What happens when the pH decreases during cellular respiration? What effect does this have on the hemoglobin’s affinity? What is the Bohr effect?

You can find the answers on this video as Leslie explains more about what happens during cellular respiration.

Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology T.V. where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 61, I’m going to be explaining the Bohr Effect. So, let’s get right into it.

Now, we’ve looked at this oxygen dissociation curve of hemoglobin in Episode 60 and, we showed how as oxygen is taken up by hemoglobin that increases the affinity and makes it easier for more oxygen to bind. As oxygen is released, it makes it easier for more oxygen to be released and, oxygen leaves the hemoglobin and goes into the tissues and is released so that, it can be used by the tissues, the muscles, and so on and so forth. You can review that in Episode 60 and, in Episode 59, I gave an introduction to the respiratory system. And, the key formula we looked at (let me write that up here in red) was:

You can revisit that in Episode 59 for a review on that. This is glucose (C6H12O6), this is oxygen (6O2) then, we have carbon dioxide (6CO2) being produced and, also water (6H2O) being produced.

Now, taking this and also looking at the oxygen dissociation curve, as carbon dioxide is produced, there’s another reaction that comes into play (and I’m going to show that over here in blue), and that reaction is CO2, carbon dioxide, plus H2O, that is going to give, and this can go both ways, that’s going to give H2CO3 and then, of course, since this is water, we can end up with H+  +  HCO3-:

This guy here (H2CO3) is carbonic acid, so, it’s an acid that’s why if it’s in water, it will disassociate and will get hydrogen ions (H+) and bicarbonate (HCO3-).

Now, when carbon dioxide is produced, that can cause the formation of carbonic acid and that’s going to release hydrogen ions. What is that going to do to the pH?

Well, of course, that’s going to cause the pH of the blood to decrease, so we’re going to decrease pH. I’m not going to go into too many details about what pH is but, that has to do with the acidity of the blood. If the pH goes down, it’s more acidic. If the pH goes up, it’s going to be more basic.

When the pH goes down, what that ends up doing is it reduces the affinity of hemoglobin for oxygen. So, hydrogen ions produced causes a reduction in pH, and that is going to influence the hemoglobin in such a way that the affinity for oxygen is going to be decreased and it’s going to release more oxygen than it normally would. This is called, or at least this is part of the Bohr Effect. And, I should put this with a capital ‘B’ because this is named after Christian Bohr who was the first person to describe this and, that is why we call it the Bohr effect.

So, decrease in pH decreases hemoglobin’s affinity for oxygen and, we get the Bohr effect. How that appears in the oxygen dissociation curve is that the curve actually shifts to the right. You can see this dotted red line here and, what that shows is we have a lower affinity for oxygen. So, for example, if the partial pressure of oxygen (PO2) is around 42 mmHg, normally, the hemoglobin would be approximately, what is that, 73-ish, 74-ish percent saturated with oxygen, however, because we have this Bohr effect and it shifts to the right at that same partial pressure of oxygen, we have a percent saturation of approximately 63 or 64. So, we get a 10% reduction by changing the pH by a certain amount. So, we reduce the pH, affinity for oxygen goes down, and that is called the Bohr Effect.

Now, this is one part of the equation that is a result of decreasing pH which is also a result of increasing carbon dioxide. This is a very important because, if you’re in the gym, you’re exercising, you’re working out, cellular respiration is happening even more and not only that but, if you’re exercising to the point you go into anaerobic respiration, you get lactic acid buildup and that of course is also an acid, that’s going to decrease the pH even more, decreasing the affinity for oxygen. And, you want that to be the case because this also means that more oxygen is going to be released. So, by producing more carbon dioxide because cellular respiration is happening even more, it decreases the acidity in the tissues, in the muscles, and when the blood passes there, it’s going to release more oxygen.

Now, there’s another equation that comes into play, and that also has to do with carbon dioxide. Because on the hemoglobin, you also have N-terminal amino groups (so, I’m going to write that here as) R – NH2. So, this is the N-terminal. And, in the presence of carbon dioxide (CO2), once again, that is going to cause a reaction where we are forming, and this is called carbamate (R – NH – COO-), plus H+:

So, we also have that hydrogen ion being produced here that of course, is going to decrease pH even more.

Now, what this carbonate is going to do, this is going to enhance deoxyhemoglobin stability. In other words, hemoglobin will be more stable in the deoxygenated form. In other words, it’s going to want to give up more oxygen, and of course, the hydrogen ion is also going to cause the oxygen release as we showed over here because you are decreasing pH, decreasing the affinity for oxygen. So, you can see carbon dioxide is doing this in two ways. It’s doing it by decreasing the pH; it’s doing it by producing carbamate and, that is going to enhance the deoxyhemoglobin stability. In other words, it’s more stable without oxygen so, it’s going to release oxygen, and you’re going to get this Bohr effect or the Bohr shift where the graph moves to the right, which is a good thing once again because more oxygen will be delivered to the muscles, to the tissues that need them.

That’s pretty much it! I hope that make sense with all these equations that we have here: cellular respiration, formation of bicarbonate by means of carbonic acid, and the formation of carbamates which enhances the deoxyhemoglobin stability.
That’s pretty much it for this video. As usual, if you want to see more of these kinds of videos, you can visit the website at Interactive-Biology.com. And, you’re going to get videos, quizzes and other resources to help make Biology fun. That’s it for now and, I’ll see you on the next one.

http://www.youtube.com/watch?v=MKGhoC1Bf-I

Click Here to Download This Video

Ever wonder how the oxygen binds to our blood cells and sent to the different parts of our body? Watch and learn with Leslie as he explains how this happens and uses the Oxygen-Dissociation Curve to describe this event.

Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology T.V. where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 60, I’m going to be talking about hemoglobin and what’s called the oxygen-dissociation curve. So, let’s get right into it.

We’ve already done an introduction to the respiratory system and we’ve shown how the heart beats and sends the blood. When the right ventricle sends the blood, it sends it to the lungs that comes back to the left atria and then, the left ventricle pumps and that sends the blood through the rest of the body.

We’ve also looked in the lungs and seen how we have the trachea going into the bronchi and then that splits off into the bronchioles, and as you can see here, that gives us the alveoli and it’s in the alveoli where we have the exchange between the oxygen coming into the bloodstream, via the capillaries that we have here, and the carbon dioxide leaving the capillaries going into the lungs and being sent from the body.

Now, when the blood comes in here, it is picking up oxygen, and the type of blood cells that are picking up the oxygen, would be the red blood cells. Here you can see a picture of a few red blood cells, of course, it’s simplified. It’s not showing the white blood cells or anything else. It’s just showing the red blood cells and these are the blood cells that pick up that oxygen.

In the red blood cells, we have special molecule. That molecule is called hemoglobin. You can see a three-dimensional image here of the structure of hemoglobin so, this is, (let me write it here), hemoglobin. This molecule, it’s actually a protein, and this protein is the protein that is responsible for picking up the oxygen.

Now, let’s go into a little more detail. You can see here, that we have these four structures. Those four structures are called, (let’s do that in blue), those are heme groups. All right, so these are the four heme groups. The special thing about these heme groups is that those are the parts where the oxygen is attracted, so, we have O2 that actually comes and binds to the heme groups. As you would imagine since we have four heme groups, we can take a total of four oxygen molecules. So, this is one oxygen molecule here, and we can have another oxygen molecule here, here, and also here. So, this hemoglobin molecule once again, has a capacity to hold four oxygen molecules.

What’s interesting about the hemoglobin is that whenever one oxygen binds to a heme group, that causes the entire hemoglobin structure to undergo a conformational change so, basically changing the site of the molecule whenever one oxygen binds. As you can see here, this is the heme group but, there’s stuff around on it, and you can imagine that it would be relatively hard for the oxygen to get in there and find the right spot.

However, when one binds, it causes a change which opens it up a little bit to make it a little easier for another oxygen to come in and bind. And, when that other oxygen comes in and bind, it causes another conformational change, making it easier for another oxygen to come and bind and, once again, once that oxygen comes and binds here, it makes it easier for another oxygen to come in here and bind to it. So, in other words, as it starts taking up oxygen, it makes it easier for it to take up more oxygen. And then, of course, the opposite will be true. If we have a hemoglobin molecule that has four oxygen attached and, for some reason it gives up one oxygen, that’s going to cause a change that makes it a little harder for the other oxygen to bind. In other words, it becomes easier for oxygen to leave. So, as oxygen leaves, it’s easier for more to leave; as oxygen binds, it makes it easier for more oxygen to bind.

As a result of this, we get a relationship that is shown in this oxygen-dissociation curve. And, what you can see here is, (we’re going to be looking at this blue line) and, as you can see here, it’s not a linear relationship. In other words, as the amount of oxygen increases, so here, we’re showing the pressure of oxygen, as the pressure of oxygen increases in the environment that the hemoglobin is in, you’re going to get more binding, making it easier for more to bind, making it easier for more to bind, and the graph is going to increase faster as you’re going to the right where you have an increased partial pressure of oxygen.

Not a linear relationship but, as some binds it becomes easier so, more bind faster and it becomes easier and it gets faster and faster until, of course, it reaches to where it’s getting saturated and, it dies off.

Now, you might be wondering why it’s not just four-levels since we only have four binding spots for the oxygen, the four heme groups. However, this is not looking at one hemoglobin molecule. This is looking at a bunch of hemoglobin molecules in a bunch of red blood cells and, overall, as some starts binding, it makes it easier and easier so, it’s going to increase faster and faster until it reaches to the saturation and then, it’s going to slow down when it reaches its full saturation.

Also, as you come in this direction, as the pressure of oxygen decreases, and oxygen starts to leave, here it’s leaving slowly but, as it starts to leave more, it’s dropping down faster, and faster, and faster, until all of the oxygen is gone.

So, this is the oxygen-dissociation curve showing once again, as you pick up oxygen, it makes it easier for oxygen to be picked up, so here it starts slow and it goes faster and faster and faster and as you release oxygen, it makes it easier for oxygen to leave and then, that goes down faster and faster. This is called the oxygen-dissociation curve.

That’s pretty much it for this video. If you want to see more videos like this and check out the other resources we have available, visit the website at www.interactive-biology.com.

That’s it for this video and I’ll see you on the next one.

http://www.youtube.com/watch?v=aoa50sd7lWM

Click Here to Download This Video

We are off to start learning from a new set of videos about another part of the human body system and here, Leslie opens a new topic with a brief introduction of the Respiratory System.

Watch and enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology T.V. where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 59, I’m going to be giving an introduction to the respiratory system. So, we’re changing gears now. We just finished talking about the circulatory system and, now, we’re going to talk about a system that is very closely linked to the circulatory system that is, the respiratory system.

So, let’s get right into it. Here, we’re looking at a bunch of ladies. These ladies are exercising. They are working out in the gym. Some of them are on the, like over here you can see we have one on an elliptical then, we have some riding exercise, bikes and lifting some dumbbells here and boxing a punching bag, punching a punching bag and there’s a lot going on right here. There’s one thing that these ladies all have in common, well, there are a number of things that these ladies have in common. They’re all attractive that’s one. They’re all exercising but, the thing that I want to focus on is that they are all breathing. I hope that make sense. They are all breathing, they are working out and in order to be able to get the energy that they need, they need to be breathing in oxygen. There are a number of things that have to happen in that process and we are going to talk about that today. So, whether you’re exercising or you’re just standing still or even if you are sleeping, you need to be breathing if you’re going to be alive of course, and we’re going to be talking about that today. So, let’s get right into it.

In order for us to have energy, there is a process that needs to happen and this process is called, ‘cellular respiration.’ Now, we’re not going to go into too much detail in terms of cellular respiration in this episode but, we are going to come back to it. The main thing that I want us to look at is the formula for cellular respiration, and that formula is:

If you’re a biologist, you’re into Biology, you’re in a Biology class, or whatever the case might be, I think, it’s imperative for you to know this formula. So, memorize this formula:

Now, let’s give some names to these bad boys. This guy over here (C6H12O6), that is none other glucose, okay so that a carbohydrate, it’s a type of sugar. O2, you should know that is oxygen. And then, of course CO2 is carbon dioxide and H2O, if you don’t know this, something is wrong, that is water. Well, maybe nothing is wrong, maybe you just never heard of it before. But, anyhow so, we have glucose that’s reacting with oxygen and the products, so these are the reactants on the left, the products on the right are carbon dioxide and water. And this right here is the general equation for cellular respiration. It is an oversimplification but, it gives you the things that are necessary and the things that are produced. Now, glucose, where do we get this from? Well, of course, we eat, right? We take in some food and we get glucose. So, let’s say we get this (glucose) from eating, oxygen, we get this from breathing, there’s oxygen in the air and, when we breathe, we bring in that oxygen that we need. Carbon dioxide, this is actually a waste product. We’re producing this but, we don’t actually use it. When we breathe, we breathe that out and that goes into the air, and that’s used by plants and plants can use that for photosynthesis. Water, do we need water? Yes, of course we need water. I’m not going to write anything right here because it’s just water. Water is essential for life and we are actually producing water in this process of cellular respiration.

In doing this entire thing, one of the things that we are making, or the main thing that we are making is energy. But, in order to make that energy, in order for us to get that energy when we’re exercising, walking, whatever we’re doing, we need to have oxygen. This oxygen needs to come in and, this is why we are breathing in, we’re taking in the air, and in the air, there is oxygen. And of course, we need to get rid of the carbon dioxide so, when we breathe that out, that is getting rid of the carbon dioxide. It’s doing some other things but, this the main function, the main functions of the respiratory system. We want to take the good stuff in, which in this case is the oxygen, and we want to take the bad stuff out, which in this case would be carbon dioxide. So, memorize this equation if you haven’t already, know what the components are and where they come from.

Let’s continue now. We’ve been looking at the circulatory system and, we’ve looked at over here, we have the heart and that heart is very important because it allows us to circulate the blood through our circulatory system and, one of the things that the heart does before it sends blood to the body is it sends the blood to the lungs. You can see here that the pulmonary vein is going away from the heart and that takes blood to the lungs, this is the lungs right here, and then, that blood takes up oxygen and comes back to the left ventricle and the left ventricle then pumps the blood via the aorta to the rest of the body. We’ve looked at that in previous episodes. If you do not remember, you can visit the section that’s right before this and you will get a review on that.

Now, what we’re going to do here, this is looking at the lungs but, it’s not looking at the lungs in detail. So, what we’re going to do is come over to this guy over here which is not showing the circulatory system but, it’s showing the respiratory system. And, you can see here we have the lungs and then, we have the mouth here, the oral cavity, which then goes into the pharynx and then, to the trachea and then, that takes us to the bronchus and the bronchioles and then, that goes into alveoli, and then, we can take this section here and you can see a larger area of the alveoli.

Not only that, we don’t only breathe in through our mouth, we also breathe in through our nose and, you can see the nasal cavity here is also leading into the pharynx which then goes the same route via the trachea and so on and so forth.

And, what I want you to notice is that when we look at this small section and, we look here at the alveoli, you can see that the pulmonary vein is coming in and then, it’s forming these capillary beds, and then, you can see the pulmonary artery is then going out. I want you to also notice the colors. Here, it’s showing red and this is when there’s no oxygen in the blood but as it comes into the capillary beds, and we are breathing in the air that’s coming in through the trachea, and the bronchus and the bronchioles to the alveoli, you can see here that when the oxygen gets in here, that can then go into the capillary beds and you see this color changing from red to kind of purplish and then to blue because it’s taking up that oxygen and then, that oxygenated blood is going via that pulmonary artery back to the heart.

There’s another thing that I want to mention here because I’m just giving an introduction so we’re going to go into more detail and all of these aspects later but, here we have the diaphragm, which is a muscle, and there are other muscles that are involved, and when those muscles contract, it causes the lungs to expand and, we breathe in air that has oxygen. The oxygen then gets taken into the blood stream and that goes back to the heart and the heart can then pump that oxygenated blood through the rest of the body.

Not only that, but, as the blood comes to the alveoli, it’s also bringing with it carbon dioxide. Remember that carbon dioxide that we made in cellular respiration, that’s bringing that carbon dioxide. That carbon dioxide can then go into the alveoli and then, when we breathe out, that carbon dioxide comes out via the alveoli and through the bronchioles and the bronchus and the trachea and then, through the pharynx and then either through the oral cavity or the nasal cavity.

So, we’re getting that bad stuff out, we’re getting the good stuff in. That is what the respiratory system is all about.

So, there you have it. That’s just kind of a brief overview. I kind of glossed over a lot of the details because I’m going to be getting into those details in future episodes.

But, for right now, I want to invite you to visit Interactive-Biology.com and, you will find more Biology videos, quizzes, games, a whole bunch of resources, you want to check them out. So, that’s it for this video and, and I’ll see you on the next one.

http://www.youtube.com/watch?v=OP4Xh4oawG8

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How do the differences in hydrostatic and osmotic pressures affect the flow of blood within the circulatory system and to the different parts of the body? What is filtration pressure and how are these affected during abnormal conditions such as having a high blood pressure?

Watch and learn with Leslie as he explains further about this topic. Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 058, I’m going to be talking about “Net Hydrostatic Pressure and Filtration Pressure.” Let’s get right into it.

Now, we’ve been looking at the circulatory system and we’ve shown that the blood leaves the heart and then, it goes via the aorta to the arteries and then, to the capillaries, to the venules, to the veins and then, to the vena cava, and then, ultimately, back to the heart. If you need a review of that, you can always check out Episode 054 where we go into more detail about that.

What we’re going to be doing today is we’re going to be looking at what happens between the arterioles, the capillaries, and the venules. That’s what we’re showing here. We have an artery leading to the arteriole and then, that goes to the capillary bed and then, that goes via the venules to the vein. What we’re going to look at is what happens specifically right here. The goal here is we want to get blood coming to the tissues delivering nutrients and so on, oxygen to the tissues and then, taking stuff away. So, taking away waste and so on.

What I’m going to do here is I’m going to simplify this a little bit. I’m going to show this like this. I’m going to take from the arterioles to the venules. I’m going to simplify it showing one arteriole that connects to one capillary, and then, that’s going to connect to one venule. I’m simplifying this significantly. Here we have the arteriole, here we have the venule, and here we have the capillary (I’m not going to put the ‘c’ here, but, here we have the capillary).

The main things that we’re going to focus on are the different pressures that we have in this setup. Now, of course the heart is pumping and the blood is coming in this direction, and then, it’s going via the capillaries. This is where the exchange happens because this is where we have the tissue and, this is where we want to get stuff delivered and we want to pick up stuff to take away from the tissues.

The first thing we’re going to talk about is ‘net hydrostatic pressure.’ I’m just going to write NHP for net hydrostatic pressure. When we’re talking about hydrostatic pressure, we are talking about pressure due to the fluids. Of course, in the blood we have fluids. In the tissue we also have fluids. The net hydrostatic pressure, as the blood is coming in here, of course there’s going to be a blood pressure because the heart is beating, it’s pumping the blood, and we’ve looked at blood pressure in previous episodes, and as the blood goes through the capillaries, there’s going to be friction that it’s encountering. It’s going to be bumping against the walls of the capillaries, and that is going to actually reduce the pressure. What we’re going to end up with is a high amount of pressure here and that’s going to drop down as we go along the capillaries. But, not only that, we have tissue here that’s filled with fluid also and that’s also going to exert a pressure on the capillaries.

The net hydrostatic pressure, we’re talking about the total hydrostatic pressure, that is going to be equal to the blood pressure, so the blood is pumping out, and we’re going to subtract the tissue pressure. So, the blood pressure, how much it’s pumping out and how much it’s pushing in from the fluids in the tissues. That net hydrostatic pressure is going to be greatest going out closer to the arterioles. So, we have a lot of hydrostatic pressure pushing out and, as we go down, and the blood is bumping against the walls and so on, that amount of pressure is going to decrease. This is what I’m illustrating here, it’s going down, going down, and when I reached to the end, we’re going to have the least amount of hydrostatic pressure which makes sense, as I said before, the blood is coming via the arteries to the arterioles. It’s coming because the heart is pumping it, and with that pumping we’re going to get a lot of pressure.

That’s going to be highest here, but, because this tube is so small, we have a tiny tube almost to the point that the blood cells can only get through one at a time. That is going to cause a lot of friction, and that is going to decrease the amount of pressure. If I take something and I push it across a surface, because there’s going to be friction with that surface it’s going to slow down. And, that’s exactly what we’re getting here. The amount of pressure is going to decrease as we go away from the arterioles and towards the venules. So, the net hydrostatic pressure is what we’re looking at here.

We’re going to get stuff leaving, but, not everything can leave. Blood cells aren’t going to leave but, water is small enough to get through the pores in the capillaries. So, water is going to leave. It’s going to take some oxygen with it. It’s going to take nutrients with it and so on. That is going to leave the capillaries which is exactly what we want because we want to deliver that stuff to the tissues or to the muscles or to whatever it is this capillary is going through. This is a good thing but, as the water is leaving, of course, we’re going to get less and less water inside the capillaries. Because of that, we’re going to have a change in osmotic pressure. Now, if you remember osmosis is the movement of water across a selectively permeable membrane. We have a selectively permeable membrane here.

What is going to happen is water leaves here, there’s going to be a little bit of osmotic pressure for water to come back in. As more water leaves, we’re going to get an increase in osmotic pressure and then, we’re going to get an even greater increase in osmotic pressure. That’s going to continue of course, and this is exactly what we’re going to see.

As the net hydrostatic pressure goes down, the net osmotic pressure is going to increase and increase and increase. When we take this together, we’re going to get the filtration pressure, (I’m going to write FP), and that’s going to be equal to net hydrostatic pressure minus net osmotic pressure: FP = NHP – NOP. These are not the official symbols. This is just what I’m writing for simplification. But, you can see that we’re going to get a filtration pressure. If we’re over here and we’re taking this hydrostatic pressure minus this osmotic pressure, we’re going to see that we’re going to have a net filtration pressure moving stuff out. That’s going to decrease as we go here to where in the center, the filtration pressure is going to be zero because we have this amount coming out and this amount going in. And, just to make that more equal, I’m just going to draw the rest of that arrow here. Then, of course, as we go down here, we have more pressure, going in, the osmotic pressure is significantly greater, so, we’re going to get a filtration pressure that’s pointing into the capillaries, moving stuff in.

So, over here, we’re moving stuff out. Over here, we’re moving stuff in. And if I were to draw a graph, I’m just going to draw a graph over this, I’m not sure why I did that as a dotted line, this is the y-axis and we’re dealing with filtration pressure, and let’s say this is the zero line. What we’re going to have is a filtration pressure that looks something like this. Here we have it moving out, so it’s going to be somewhere around here, and of course, that’s going to go down to zero at this point, and then, continue going down, showing that we have a negative filtration pressure or in other words, a pressure moving stuff into the capillaries. Here is ‘moving out of’ and here we’re ‘moving stuff into.’

This point right here, where we have a filtration pressure of zero, that is called the ‘dynamic center.’ This is where the net hydrostatic pressure is equal to the net osmotic pressure — equal but, and opposite of course — and that is called the dynamic center. In a perfect world, this dynamic center is exactly where we want it to be so that, we have a good amount of distance for stuff to leave and a good amount of distance for stuff to come in. So, we’re delivering the nutrients and the stuff that we need to the tissue, and we’re taking away the waste and the stuff that we don’t want sending that away from the tissues.

I want to look at a different scenario, where we have the same setup. We have the arteriole, the capillary and the venule going back to the veins, and vena cava, and back to the heart. But, in this situation, we’re going to be dealing with someone that has high blood pressure. So, here, we’re going to have a significant amount of net hydrostatic pressure pushing stuff out. So, it’s much higher. What that’s going to do, as you can see here is the pressures are going to be greater all the way along. Yes, it’s decreasing but, because we’re starting with a higher amount, we’re also going to end with a higher amount.

We also have the osmotic pressure doing the same thing that it was doing before and, stuff is leaving, and let’s say, we have it here, and this is kind of extreme and let’s say that because of this high blood pressure, we still have the filtration pressure here, we have the osmotic pressure here. But, the dynamic center, instead of being over in the center, the dynamic center is somewhere around here. Now, that is a significant problem because this is what we have. In this entire section we have this fluid leaving and, it’s not until here that we have a net amount of fluid coming in. What’s that going to do is it’s going to cause more fluid to be leaving than the amount of fluid that’s coming in, and that is going to result in accumulation of fluid in the tissues or, we can also call that, edema. So, this can be a result of high blood pressure because we have more fluid leaving the capillaries than coming into the capillaries. We have more going towards the tissues and that can cause a significant amount of problems resulting in edema.

So, the take home message, net hydrostatic pressure is blood pressure minus tissue pressure. That’s what we’re showing here. And, if we want to find the filtration pressure, we take net hydrostatic pressure minus net osmotic pressure. That will give us that filtration pressure. To this side of the dynamic center, the filtration pressure is moving fluids and dissolved molecules out of the capillaries. As we come to this side, it’s moving fluids into the capillaries. If we have high blood pressure, that can shift the dynamic center significantly resulting in accumulation of the fluids in the tissues or edema.

That is pretty much it for this episode. As usual, I’d like to invite you to visit the website at Interactive-Biology.com for more Biology videos and other resources. That’s it for this video and I’ll see you on the next one.

http://www.youtube.com/watch?v=DfAyZwsIYR4

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Here is an interesting concept about pressure reflexes that you might want to watch. It is related to the mean arterial pressure of a man. Learn more by watching another one of Leslie’s easy videos to help you understand these concepts easier.

Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 57, I’m going to talk about, ‘Pressure Reflexes and Mean Arterial Pressure.’ We’ve been talking about mean arterial pressure a lot, we’ve spoken about cardiac output and peripheral resistance. You can always revisit previous episodes to find out more about them.

Today, we are talking about pressure reflexes. We’ll look exactly at why we call it pressure reflexes. Here we have the heart (I feel like I keep saying that in very episode recently) and the heart, it pumps the blood throughout the body. We have the aorta.

One of the arteries that I have not been talking about would be the carotid artery. This is the common carotid. I’m just going to come here and draw a line here and say, that we’re dealing with carotid arteries. Of course, here, we are dealing with the aorta.

There is something very special that we have in these two arteries. In both the aortic and the carotid bodies, we have receptors that we call ‘baroreceptors.’ From the time you hear the prefix ‘baro-,’ you should know that it has something to do with pressure. For example, a barometer measures pressure and, here we have baroreceptors and these baroreceptors respond to changes in, you guessed it! Pressure. That is why they are called baroreceptors.

What’s going to happen is, if we have an increase in the mean arterial pressures, so we have a significant increase in mean arterial pressure, what that’s going to do, these baroreceptors are going to start firing. We’re going to have an increase in the firing of these baroreceptors. In other words, they’re going to be sending signals. Those signals are going to a region in the brain stem that we call the medulla. This is known as the “blood pressure regulating center.” Of course, it regulates other things but, it also regulates pressure.

That then, is going to cause a combination of two things. It’s going to cause an increase in parasympathetic activity and going to cause naturally a decrease in sympathetic activity. If you remember from one of the early episodes, sympathetic activity causes stuff like increase in heart rate, increase in blood pressure, and so on. Parasympathetic activity calms stuff down so, it reduces blood pressure, it reduces heart rate, breathing rate, and so on. So, we have an increase in mean arterial pressure, so an increase in blood pressure, the baroreceptors are going to respond by sending signals to the medulla. That’s going to cause an increase in parasympathetic activity, calming stuff down, and a decrease in sympathetic activity. Sympathetic activity would normally increase pressure, and speeds stuff up but, here we’re slowing that down. So, the net result of these two things is we’re going to get a reduction in cardiac output and also in peripheral resistance. Then, of course, that is going to cause a reduction in mean arterial pressure.

This is why we call it a reflex because we have an increase in mean arterial pressure, and that’s going to cause a number of things that’s going to eventually cause a reduction in mean arterial pressure. The relationships between these quantities here, we’ve looked at a number of times, and, just to revisit that:

M.A.P. =CP x PR,

Mean arterial pressure is equal to cardiac output times peripheral resistance. Since we’re decreasing both cardiac output and peripheral resistance, we are also going to decrease mean arterial pressure.

That’s pretty much it for this episode. Of course, you can always visit the website at Interactive-Biology.com for more Biology videos, more Biology resources, and more Biology fun. That’s it for now and I’ll see you in the next one.

http://www.youtube.com/watch?v=MRcra9oxrXY

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Here is the second part of Regulating Peripheral Resistance. Leslie explains two more ways on how it can be influenced and how it affects someone’s blood pressure and mean arterial pressure. Watch to learn more!

Have fun!

Transcript of Today’s Episode

Hello and welcome to yet another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 56, I’m going to continue talking about, ‘Regulating Peripheral Resistance.’ This is part 2, and I think this is going to be the final part about this. So, let’s get directly into the content for today.

In the last episode, we emphasized, we re-emphasized the fact that mean arterial pressure is equal to cardiac output times peripheral resistance (M.A.P. = CO x PR). We’ve spoken about the fact that we are modifying peripheral resistance. We’re looking at the different ways in which peripheral resistance is influenced. In the last episode, you can go back to Episode 55, we spoke about vasoconstriction and we said that that is going to cause an increase in peripheral resistance. We spoke about vasodilation which is going to cause a decrease in peripheral resistance.

We’re going to talk about two other ways in which we can influence peripheral resistance. The first way that we are going to talk about today is called, blood viscosity. By viscosity what I mean is basically the thickness of the blood. This is very logical.

For example, a few weeks ago I was in Colombia and we remember we went to a restaurant and I ordered a mango milk shake. The milk shake was very, very, very thick. I was sucking on the straw trying to get it out and it was really hard to get that mango, I mean it was a very good tasting mango milkshake but, it was hard to get it in my mouth because of how thick it was.

This is the same thing. The thicker the blood is, the more resistance we’re going to have to blood flow. If we increase blood viscosity, we’re going to increase peripheral resistance significantly. By the viscosity, specifically, I am talking about the ratio of RBCs (red blood cells) to the blood plasma:

RBCs : plasma

By plasma, we’re basically talking about the fluid. If we have more red blood cells, or we increase the ratio of red blood cells to plasma, we are increasing the thickness of the blood. So, the overall message is, and let me just divide this in two, if we increase blood viscosity, that of course is going to result in an increase of peripheral resistance. On the other hand, if we (let’s use a different color), decrease blood viscosity, that is going to cause a decrease in peripheral resistance.

What is an example of a way we can increase blood viscosity? Well, for example if we are dehydrated. What that’s going to do is it’s going to reduce the amount fluid in the blood, so the plasma is going to be less. That is going to cause an increase ratio of red blood cells to the plasma, we’re going to have an increase in blood viscosity, and that’s going to cause an increase in peripheral resistance.

What can cause decrease in blood viscosity? For example, loss of blood volume due to anemia or if there’s hemorrhage, that’s another example (forgive my R’s… My students always make fun of me for my R’s). If there’s anemia or hemorrhage, that’s going to cause a decrease in blood viscosity causing a decrease in peripheral resistance. So, the first that we’re looking at today is by influencing blood viscosity.

The second way is by looking at the total blood vessel length. The message here is, the longer the blood vessels, the higher is the peripheral resistance. So, if you increase the blood vessel length, you are going to naturally increase peripheral resistance. That should also make sense. If something is much longer, you have a tube that’s very long, it’s going to be much harder to get the blood through. If my straw for my mango shake was extremely long, let’s say that straw was two-feet long, that would take a lot of work for me to get that great tasting mango shake into my mouth because it’s longer, increase in peripheral resistance.

Now, how would this translate to the human being? I’ll give you a very good example in America and other places also. If someone is overweight, what that’s going to do is that’s going to naturally increase blood vessel length. I’m going to give you some numbers right now that can be very disturbing. Or, it can’t be very disturbing depending on how you look at it. If you gain 2.2 pounds of weight of additional fat, that is going to add approximately, and this is very scary, 400 miles of blood vessels. That’s one kilogram of fat and approximately 650 kilometers of blood vessels. So, you can see, by gaining weight, you’re gaining more blood vessels. That’s basically increasing the blood vessel length, and that is going to increase peripheral resistance. And we know what increase in peripheral resistance will do to mean arterial pressure and to blood pressure because, we keep coming back to this:

M.A.P = CO x PR

More fat, longer blood vessels, increased peripheral resistance, and that is going to cause an increase in mean arterial pressure.

I guess, the take home message for today is, watch your weight.

That’s pretty much it for this episode. As usual, I want to invite you to check out the website at Interactive-Biology.com for more Biology videos and other resources. You can join the community over there, ask your questions in the forums, and just take part in everything that we have going there. That’s it for this video and I’ll see you in the next one.

http://www.youtube.com/watch?v=14Z8GNLU4os

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As promised, here is a video focusing on peripheral resistance. Understand what it is and how it affects mean arterial pressure by watching along and listening as Leslie once again explains the concept with full clarity.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel, and in this episode, Episode 55, I’m going to be talking about, ‘Regulating Peripheral Resistance,’ and this is going to be part 1. Initially, I was going to make one video about peripheral resistance, but, then I started going into it and I decided to split it up into at least two parts. So, this is going to be the first part. It might end up being two parts, it might end up being three parts. We’ll see how it all turns out.

We’ve been talking about the cardiovascular system or the circulatory system. We have spoken a lot about the heart and the blood vessels that lead from the heart and to the heart. We said that when the heart beats, and let’s say the ventricles contract, that sends the blood, if it’s the left ventricle, it sends the blood into the aorta which then sends the blood into the rest of the body. It’s going to the organs, and to the tissues. It’s taking oxygen and nutrients to the organs and the muscles, and so on. And, of course, it’s bringing waste away from the muscles and organs also.

What we’re going to do today, we’ve been talking about cardiac output, we’ve been talking about the mean arterial pressure and in the last episode, we focused on mean arterial pressure and we said that:

M.A.P. (mean arterial pressure) = CO x PR

This is one of the formulas that we use for calculating mean arterial pressure. Just as a reminder, the other one is:

M.A.P. = Diastolic pressure + 1/3 (systolic pressure – diastolic pressure)

You can go back to Episode 54 for more of an explanation on this two. We’re not going to focus on this guy right here. We are focusing on this indirectly. Why? Because today, we’re going to talk about peripheral resistance. We already defined what peripheral resistance is. Peripheral resistance is basically opposition to blood flow. Of course, you have the heart that’s beating and sending the blood through these blood vessels. But, of course, it’s not a frictionless environment. There’s going to be friction between the blood and the walls of the blood vessels that is going to cause resistance. If something is trying to get through a tube, there is resistance. This is exactly what we have here, the blood is trying to get through many tubes all throughout the body. Of course, that is going to encounter resistance. Just to give you an idea, if you were to take all of the blood vessels out of your body and just make it in one long line, it would be long enough to wrap around the globe twice. So, we have a significant amount of blood vessels going through the body. That is what peripheral resistance is.

What we are going to do is we are going to talk about how we can regulate peripheral resistance. So, I said, we have the heart and that sends the blood to the rest of the body. There are a number of different types of vessels that we can encounter. We have, of course, the aorta, and we’ve looked at this. From the aorta, it’s going to go to the arteries. From the arteries, it’s going to go to arterioles, and from the arterioles, it’s going to go to the capillaries, and then, from the capillaries, (let’s use a different color here), that’s going to take us to the venules, to the veins, and then, via the vena cava, and then, that is going to go back to the heart. That cycle continues.

When it comes to peripheral resistance, the place that we’re going to focus on will be the arterioles. The aorta and the arteries are relatively thick. Yes, they are flexible but, we don’t have much in terms of changing the diameter of these guys. The arterioles has a smooth muscle layer, a significant smooth muscle layer, that we can constrict or we can dilate. If we constrict it, the diameter is going to be smaller. If that’s the case, that is going to increase peripheral resistance. If we expand it, if we relax the muscles, we dilate the muscles, the arterioles are going to expand, and, of course that is going to decrease peripheral resistance. It’s really simple. It is harder to get something through a very narrow tube than it is to get something through a thicker tube. So, by constricting the arterioles, that is going to increase the peripheral resistance; by dilating the arterioles, that is going to decrease peripheral resistance. Just to give you a visual here. Here we have an artery. We’re delivering blood to a specific tissue whatever that is. So, we have some tissue cells here. From the arteries, it goes via arterioles and then, we have the capillaries going to the venule and then, to the vein, and as I said before, then back to the vena cava and back to the heart. The magic is happening right here in the arterioles. If we have some constriction, that is going to increase peripheral resistance. If we have dilation, that’s going to decrease peripheral resistance.

Now that we know that, let’s talk about some specific instances and some specific ways in which we can have these kinds of effect.

We’re going to look at two hormones. We’re going to look at epinephrine which is another name for adrenaline, and you’ve heard a lot about adrenaline. And, we’re also going to look at norepinephrine. So, these are the two that we’re going to look at today.

First, we’re going to focus on epinephrine. The interesting thing about these things, I’m going through one example of one pathway for each but, epinephrine, for example, in certain instances, it can be a vasoconstrictor. In other instances, it can be a vasodilator. What we’re going to do, the typical one that you hear about is the vasoconstriction. I’m going to talk a little bit about how this causes vasodilatation.

Epinephrine binds to what we call, beta-2 receptors and these are on the smooth muscles of the arterioles and then, what that’s going to do is it’s going to activate a G-protein which then is going to activate an enzyme called adenylate cyclase. What this enzyme is going to do, it’s going to take ATP, adenosine triphosphate, which is the energy currency of the body and convert that into a different form. That’s going to be a cyclic AMP. What that’s going to do is it’s going to activate calcium pumps in the cisternae of the smooth muscle cells. That is going to cause the calcium to be pumped back into the cisternae which is going to decrease calcium level. So, we’re going to get calcium decrease. If you remember from one of the earlier episodes, calcium in the muscle causes muscle contraction. If we’re decreasing the calcium, we’re not going to get contraction which would cause constriction. We’re going to get vasodilation. When we have vasodilation, of course, what that’s going to do is it’s going to decrease peripheral resistance because we have a wider tube, blood can flow much easier. So, that’s going to cause a decrease in peripheral resistance. This is one example of one way in which epinephrine can affect peripheral resistance.

Let’s talk about norepinephrine. (Let’s come over here). Norepinephrine is going to activate a different type of receptor. We’re going to call those alpha-receptors. That is going to activate a G-protein, once again. However, in this case, the G-protein is not going to activate adenylate cyclase. It’s going to activate phosphatidylinositol and then, that is going to activate the molecule IP3. That is going to do the exact opposite. That is going to cause calcium release from the cisternae. Of course, now, we have calcium release that is going to cause contraction which in this case would be vasoconstriction. Of course, then, the effect of that is going to be to increase peripheral resistance.

We’ve been looking at the formula: M.A.P. (mean arterial pressure) = CO x PR. In these situations, we are affecting PR, which is peripheral resistance and if you increase peripheral resistance, which would be the effect of norepinephrine in this specific situation, that is going to cause an increase in the mean arterial pressure. If you decrease peripheral resistance as in this situation, that is going to cause a decrease in mean arterial pressure.

So, by influencing vasodilation or vasoconstriction, what we’re doing is we are making the diameter of the blood vessels smaller or larger. That is going to influence peripheral resistance. If it’s smaller, we have more resistance. It’s harder to get stuff through. If it’s larger, it’s going to be easier to get stuff through because there’s less resistance to flow.

There’s one more thing that I want to add to this. Here we have an example of atherosclerosis and that is where we have plaque buildup in the arteries. So, here you can see the plaque, and that is building up in the arteries. What that’s going to do is, it’s going to cause for us to have a narrowed arteries. So, the diameter is going to be significantly smaller. This can happen as a result of having too much cholesterol in our diets. That’s just an example but, that is going to cause a smaller opening. Of course, if you have a smaller opening, what that’s going to do is, it’s going to increase peripheral resistance. If you increase in peripheral resistance, and we know that:

M.A.P. = CO x PR,

You increase this over here, that is going to increase the mean arterial pressure. So, you’re basically increasing the blood pressure when there is plaque in the arteries. You’re doing that by increasing peripheral resistance.

Take home message is: Watch your diet, exercise, live a healthy lifestyle, so that this doesn’t happen, so that this doesn’t go up and so that your blood pressure, your mean arterial pressure does not go up. That’s the health nugget for this lesson.

That’s pretty much it for this episode. As usual, you can visit the website at Interactive-Biology.com for more Biology videos and other resources that we’re adding over there. This is Leslie Samuel. Thank you for watching and I’ll see you on the next one.

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What does blood pressure really mean? What does it actually measure? Watch, listen, and learn as Leslie once again explains clearly and makes it so simple for everyone of us to understand easily about the principles behind this new episode.

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Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel, and in this episode, Episode 54, I’m going to be talking about ‘Blood Pressure and Mean Arterial Pressure.’ These are the two things I’m going to cover today. Blood pressure… You know, when you go to the doctor’s office, one of the first thing they do is they take your blood pressure. And, you know what? After today, you’re going to know exactly what they’re doing and what it means, if you don’t already know. So, let’s get right into the topic for today.

Here, we have the heart. We’ve been speaking about the heart because we’re talking about the cardiovascular system or the circulatory system and the heart has a very important job. It’s pumping the blood throughout the body. The blood carries oxygen and nutrients to the muscles and to the other organs that need this in order for you to live; in order for you to do all the things that you are doing right now.

Here is the heart. If we take the heart and we put it inside the human body, you can see here, we have the human heart and it is serving the purpose of pumping the blood through these arteries, to the rest of the body. Of course, the blood is coming back via these veins to the heart. That process goes over and over. It’s also sending the blood to the lungs so that it can get the oxygen that it needs and then send that to the body and so on. We’ve kind of spoken about that in previous episodes.

Today, we want to talk about blood pressure. First, I’m going to define blood pressure and I’m going to do it simply by writing here. Here, we have the blood and over here, we have blood vessels. As the heart is beating, and it’s sending that blood out to the body, it’s going via these blood vessels, and because it’s being pumped, that is going to exert a pressure on the blood vessels. We’re going to call this pressure a ‘hydrostatic pressure.’ The reason we call it a hydrostatic pressure is because blood is a fluid, and when fluids exert pressure on something, that is called, ‘hydrostatic pressure.’ Okay, so, the blood is being pumped. It’s going through these blood vessels. It’s hitting against the walls of the blood vessels, the inner lining of the blood vessels. That is exerting a pressure on those blood vessels. This is what we mean when we say ‘blood pressure.’

When the doctor is taking your blood pressure, or the nurse is taking your blood pressure, they are checking to see how much pressure is exerted on the blood vessels by the blood. That is a very important measure when it comes to the health of your body.

When the blood leaves the heart, as we’ve shown before, the blood then goes into the aorta which is this vessel that’s leaving from the heart, and then, that goes down here. This is also the… this is called the descending aorta and it goes via these other blood vessels to the rest of the body. It would make sense to understand that the closer you are to the heart, the more you’re going to feel that pressure. If you are right by the heart, you’re going to feel more pressure than if you are all the way down here in the toes, right? Because here is where the heart is beating, and the farther away you go from that, the lower the pressure is going to be.

Let’s look at how this works. What I’m going to do is I’m going to draw a little graph here. (I just realized that I can use a ruler on my tablet which makes sense but, I just never thought about it). Here we have the y-axis and then, here, we are going to draw the x-axis. What I’m going to do is kind of chart the blood pressure as the blood is going from the heart to the, first it’s going to go via the aorta (let me write ‘aorta’), and that’s right here. As it leaves the aorta, it’s going to go to some little smaller vessels and those are called arteries. From there, it’s going to go even smaller to the arterioles. From there, it’s going to go to the capillaries (I’m just going to write here ‘cap’). That is where it actually crosses over from being in the arteries section, arteries and arterioles, to where it’s going into the veins. But, before it goes to the veins, it’s going to go via the venules and then, the veins. When it’s in the venules and the veins, it’s because it’s going back to the heart eventually via the vena cava.

We’re going away from the heart via the aorta and then, we go to the arteries. We’re going away — a very easy way of remembering this is the ‘a’ in ‘arteries,’ ‘arterioles,’ and ‘aorta’ is going ‘away’ from the heart. When it reaches the tissues and the organs, it’s going to have an exchange in the capillaries where it then goes into the venules, to the veins, and then, back via the vena cava to the heart.

Let’s look at pressure on the y-axis. I’m going to give these some values of 20 (let me just write them in here first. Okay, it’s not fully evenly spaced), 20, 40, 60, 80, 100, 120, and 140. On the y-axis we’re dealing (I’m just going to write it over here), with pressure in millimeters of Mercury (mm Hg).

When the heart contracts, we have ventricular contraction and that’s when we’re going to get the greatest amount of pressure because the ventricles are larger than the atria. When they contract sending the blood to the rest of the body, that’s going to give you the systolic pressure, which is going to be the greatest pressure. We’re going to see here, (let me draw this in… Let’s go with red), the ventricles are contracting so the pressure is going to increase significantly and then, as the atria contract, you’re going to get that little bump there. That process continues as the heart beats, continues as the heart beats. We’re in the arteries.

As we go away from the arteries and into the arterioles, what you’re going to see, we’re getting away from the heart a little bit, the pressure is going to start kind of going down, going down. As you go away, you’re going to see smaller fluctuations. You’re not getting as great of an effect. As we reach into the capillaries, it’s kind of dying down even more and the pressure is going to continue going down and down until, on the way back to the heart, there’s hardly any pressure remaining. I mean, in comparison to up here, where we had pressures of up to 120 mm Hg, or sometimes even more in this situation, in comparison, the farther away we get from the heart and as the blood is being pushed back to the heart, we don’t get these fluctuations in pressure and there’s significantly less pressure as the blood is going back to the heart.

When the doctor takes your pressure and the doctor says, “You are in excellent health. Your blood pressure is great,” what are the numbers that you usually hear? The numbers that you usually hear are 120 over 80 (120/80). What that refers to, of course at the top, we have the systolic pressure and here we have the diastolic pressure – systolic pressure and diastolic pressure. Systolic is during systole contraction so, that’s the higher point. Diastolic is during relaxation where we have a lower point. If you have that 120/80, you are a happy camper. All is well with the world, at least where your blood pressure is concerned. That is what we want to have.

That is blood pressure. When you’re measuring blood pressure, you’re measuring the difference between systole and diastole – contraction and relaxation.

Now, let’s talk a little bit about ‘mean arterial pressure.’ (I’m just going to write M.A.P. for short). Mean arterial pressure, when you hear the word ‘mean,’ you always think average. The mean arterial pressure is basically the average pressure in the arteries. We’re not looking at the fluctuations. We are looking at the average. If we were to take the average here, I’m just going to plot a second line, it would look something like this. So, straight line here and as it goes down, it’s going to look a little like this until where we have a straight line here, it follows that straight line. That gives us the average pressure in the arteries.

There’s a formula that we use to calculate mean arterial pressure. Mean arterial pressure, M.A.P., is going to be equal to CO times PR.

M.A.P. = CO x PR

Now, two of these you know already: M.A.P., mean arterial pressure; and CO, you should know that that is cardiac output. PR is one that we haven’t covered. PR is ‘peripheral resistance.’ As I said,

M.A.P. = CO x PR

We’re going to go more into peripheral resistance in the next episode so, I’m not going to deal too much with this. The main thing that you want to know is the two factors that are going to influence mean arterial pressure is cardiac output and peripheral resistance. Peripheral resistance is basically, we’re going to define that as, opposition to blood flow. The blood is flowing but, of course there’s going to be some resistance, there’s going to be friction between the blood and the walls of the blood vessels and so forth.

There’s another way of calculating mean arterial pressure. Mean arterial pressure is also equal to diastolic blood pressure, so, that’s during diastole, relaxation, plus 1/3 times systolic blood pressure minus diastolic blood pressure (my handwriting is getting kind of sloppy there but, you get the point).

M.A.P. = diastolic BP + 1/3 (systolic BP – diastolic BP)

Once again, if you’re looking at that graph where we had something kind of looking like this, in the beginning, and if this is 80 and this is 120, the mean arterial pressure is going to be equal to 80 plus 1/3 of 120 minus 80, is 40, and that’s going to be equal to 80 plus let’s see, 1/3 of 40, let’s go with 13.3, I’m just going to leave that at 13, so, mean arterial pressure would be equal to 93 mm Hg.

M.A.P. = 80 + 1/3 (40) = 80 + 13 = 93

That’s mean arterial pressure. Two ways to calculate it: Cardiac output times peripheral resistance. We’ve dealt with cardiac output, that’s the amount of blood pumped by the heart every minute and we’re multiplying that by peripheral resistance which is the opposition to blood flow. In Episode 55, we’re going to go a little more into peripheral resistance or, we can take the diastolic blood pressure plus one-third of the difference between the systolic and diastolic blood pressures which in this case would be 80 plus a third of 40 which would be approximately 13, which gives us 93 mm Hg:

M.A.P. = 80 + 1/3 (40) = 80 + 13 = 93 mm Hg

That’s pretty much it for this episode. Of course, if you want to check out some more Biology videos and other resources like quizzes and the community that we have at Interactive-Biology, you can check out the website at Interactive-Biology.com.

That’s all for now, and I’ll see you on the next one.

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Learn more about calculating cardiac output and how changing stroke volume and heart rate can increase or decrease its value.

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Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel, and in this episode, Episode 53, I’m going to talk about the ‘Cardiac Output.’ I’m first going to talk about what it is and then, I’m going to talk about how to calculate it, and some of the things that are going to influence cardiac output. So, let’s get right into it.

Here, we’re looking at a picture of the heart. A diagram of the heart during systole, so it’s during contraction, ventricular contraction, and what’s happening here, is as the ventricles contract, the left ventricle is sending blood to the aorta which then goes to the rest of the body, the right ventricle of course, is sending the blood to the lungs so that, it can get oxygenated, come back to the heart and then, be sent to the rest of the body.

Now, we’re going to talk about cardiac output today so, let me write that here, ‘Cardiac Output.’ It kind of is exactly what it sounds like. Cardiac output is talking about the volume of blood that’s being ejected from the ventricles every minute. So, we’re talking about the amount of blood that’s being sent from the left ventricle to the rest of the body via the aorta, and also we’re talking about the amount of blood that’s being sent from the right ventricle to the lungs. You expect those to be the same or else that can lead to some other problems. That we’re not going to get into in this episode.

Right now, we are just going to try to look at how to calculate cardiac output. It’s a pretty simple formula and it involves two things that we’ve already looked at in previous episodes. Cardiac output is equal to SV, which is stroke volume, times HR, which is heart rate:

CO = SV x HR

Now, stroke volume tells you the amount of blood that’s ejected with each beat. So, we’re talking about milliliters of blood per beat, and then, with heart rate, we’re talking about how many times the heart is beating in one minute. So, we calculate that as beats per minute. So, stroke volume is the amount of blood ejected from the ventricles, let’s say the left ventricle in each beat, with each beat. And, the heart rate tells us how many times the heart is beating, how many times the ventricles are contracting in one minute. If we, multiply these out of course, if you apply some simple algebra, we’re going to be canceling out the beats, so, cardiac output is calculated in milliliters per minute – some pretty straightforward algebra there.

Now, let’s plug in some values. The average adult male has a stroke volume of approximately 70 millliters per beat and an average heart rate of 75 beats per minute. Now, if you want to calculate cardiac output, the amount of blood ejected from the ventricle each minute, cardiac output would be equal to 70 milliliters per beat times 75 beats per minute and that’s going to give us a value of 5,250 milliliters per minute. Of course, you can make that into 5.25 L per minute. So, this is the average adult male at rest, 5.25 L/min cardiac output. Now keep in mind that the average adult male has about 5L of blood in their body. So, every minute the heart is re-circulating pretty much all of the blood if you’re just at rest. All right, so the heart is doing a significant amount of work. It’s sending the blood to the muscles, that organs that need to get oxygen and the nutrients that come via the blood.

We know how to calculate cardiac output. Now, if you want to change cardiac output or if you want to influence cardiac output, it should be obvious that we can do that in three ways by influencing stroke volume, by influencing heart rate, or by influencing both of them. So, if you make a change, to the stroke volume or the heart rate, that of course, in turn is going to make a change to cardiac output.

Now, we’ve also looked at factors that are going to influence volume and heart rate. We’ve spoken about those factors in Episodes, I think it’s 46 and Episode 50. Episode 46 talks about how we can influence heart rate. Episode 50 talks about influencing stroke volume. You can always revisit those and see how that works.

When you’re exercising, you’re going to have a little bit of a different situation. You know when you’re starting to exercise and you’re doing some aerobic activity, your heart rate is going to increase, your cardiac output is also going to increase because you’re increasing stroke volume and your heart rate so, that’s going to give you some different values.

Let’s take an example where we’re trying to calculate cardiac output again. As usual, cardiac output is equal to stroke volume. We’re going to take that and multiply that by heart rate. Same exact situation.

CO = SV x HR

But, okay, I’m showing ladies here exercising but, we’re going to stick with the example for the calculations, we’re going to stick with males, and we’re going to see during moderate exercise, the stroke volume might increase to a point of let’s say about 100 mL/beat, and let’s say the heart rate increases before it was 75 and let’s say we have, let’s go with a 100 because that’s easy to calculate, a hundred beats per minute (100 beats/min). So, we have more of an intense situation, it’s not a very stressful situation but, you’re doing some exercise. So, that’s going to influence cardiac output of course. Cardiac output is going to be equal to:

CO = 100 mL/beat x 100 beats/minute

Giving us a cardiac output of 10 L/min. So, by doing a little bit of exercise, we’ve almost doubled the cardiac output. In other words, your blood is being pumped throughout your body twice in that minute with moderate exercise.

As you exercise and you train, hopefully we’re doing this on a regular basis, hopefully, like three times a week, **hint, hint, hint** but, as you’re doing this more regularly, there are going to be some adaptations that happen. One of the main adaptations is that your stroke volume increase, (I’m just going to put an up arrow here showing that your stroke volume increases). In other words, everytime that your heart pumps, it pumps more blood than the average untrained individual.

What that can do in turn is that can actually cause a lower resting heart rate. All right, so, a trained person on average has a lower heart rate than an untrained person. However, they’re still able to get the same cardiac output. In other words, your heart is becoming more efficient at pumping the blood. Everytime it contracts the ventricles, it’s sending a significant amount more than the untrained person and you can achieve the same effect if not even a better effect with less work.

So, the take home message there I guess you could say is, do like this ladies, get into the gym and start doing some exercise. That’s always good and it’s going to pay off in the long run.

That’s not what I intended to teach but, hey it’s something that’s good for us to learn. That’s pretty much it for this episode. As usual, you can visit the website at Interactive-Biology.com for more Biology resources and a bunch of other resources that we’re adding there. We’re adding quizzes and we have just added a brand new Biology community where you can ask questions, get answers, give input. Join the community and make the community stronger and much more fun.

Thank you for watching this episode and I’ll see you on the next one.

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Ever wonder what happens in a heartbeat? What happens inside our heart when we hear the ‘lub-dub’ sound?

Watch and see as Leslie describes in full detail what a cardiac cycle is and how this is reflected in one heartbeat.

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Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel, and in this episode, Episode 52, I’m going to be talking about the ‘Cardiac Cycle.’ When I say the cardiac cycle, I’m talking about all of the events that happen with one complete heartbeat. So, we’re going to go into the details of this. There are a lot of details but, we’re going to try to break it down, one step at a time to make it as easy and as fun as possible. Let’s get right into it.

Here, we are looking at the entire cardiac cycle. We have this graph here that shows a number of details and, to make this as easy as possible, what we’re going to do is we’re going to take everything and break it down one section at a time. I want you to follow me on this. Like I said, we’re talking about one complete heartbeat and with one complete heartbeat, I’m talking about the contraction and the relaxation of the atria and the contraction and the relaxation of the ventricles. Anytime I say contraction, I’m referring to systole which is the CMS contraction; and, when I say relaxation, I am referring to diastole.

What we’re going to do is first, I’m going to describe what all these things show, and then, we’re going to take it one stage at a time.

Here, we’re looking at the phonocardiogram. In other words, we’re looking at the sounds that we hear when the heart beats, when we’re looking through the different stages of the heartbeat. Then, here we’re looking at the electrocardiogram, and we’ve looked at that in a previous episode. You can always revisit that to get a good understanding of how the electrocardiogram or the ECG or the EKG works.

Then, we’re looking at the ventricular volume. In other words, we’re looking at the amount of blood, the volume of blood in the ventricle, specifically we’re looking at the left ventricle. Then, here in blue, we are looking at ventricular pressure. So, that’s the pressure in the left ventricle. Here in gray, we’re looking at the atrial pressure, so, the pressure in the atria. Then, last but not least, we’re looking at the aortic pressure, and that’s the pressure in the aorta which is this structure right here, which sends the blood from the heart to the rest of the body.

That’s an overview of what we’re going to be looking at. Now, we’re going to take it one section at a time. This has a lot of details in it. It summarizes the entire cardiac cycle so, we’re going to take it one step at a time and get a good understanding of what is going on. Actually, I am going to start right in this section here. The reason I’m going to start here is because here we have showing the P, Q, R, S complex and the T wave. This is one full cycle but, this is labeled differently so, we’re going to look at that.

I’m going to start by looking at the electrocardiogram. First thing we’re going to see is we have the P wave, and if you remember from a previous episode, the P wave represents atrial depolarization. So, we’re talking about the depolarization of the atria. Once this happens, that is going to cause the atria to contract. So, let’s jump up here and look at the atrial pressure. You can see here, right after the P wave we get this increase in pressure in the atria. That is when the atria are contracting and that is why we see that increase in pressure as a result of the depolarization of the atria. Once again, the P wave represents atrial depolarization that is going to cause atrial contraction or, as you can see here, atrial systole. What that’s going to do is that’s going to push the last bit of blood from the atria, which is this part over here (I’ll show it with a blue pointer), from the atria into the ventricle. So, we’re going from the left atria, left atrium to the left ventricle when that contracts. That is why we see this quick increase in the amount of blood in the left ventricle. So, we get an increase in ventricular volume right after the atria contracts.

We’ve described this section here which is the atrial systole. And then, after the P wave, we then get the QRS complex. Once again, we’ve covered this in a previous episode, I think it’s Episode 48 where we talked about the EKG. The QRS complex represents the depolarization of the ventricles. And of course, once the ventricles depolarize, that’s going to cause the ventricles to start to contract just like after atrial depolarization, we get atrial contraction.

Now, after ventricular depolarization, we also get ventricular contraction. So, that is where we’re starting this phase of systole where the ventricles are contracting. However, there is a short period here, and you can see here the same period. It’s called isovolumic or isovolumetric contraction. That is when these valves, the atrioventricular valves and the semilunar valves are closed as there’s a buildup in pressure. You can see there’s a significant increase in pressure here during the stage of isovolumetric contraction. Of course, the volume of blood in the ventricles is staying the same. So, here, you see the left ventricular volume is staying the same. At a certain point, we will have enough pressure in the ventricle to cause the semi-lunar valve to open so that you can pump the blood into the aorta. Now, at what point is that? Well, you can see here the aortic pressure is somewhere around 80 mm Hg as you can see here. So, once we have enough pressure to overcome the pressure in the aorta, that’s going to cause the valve to open, and then the blood can be sent to the aorta which can then go to the rest of the body.

In the case of the ventricular volume, when those valves open, and the blood leaves, that’s going to cause the ventricular volume, the amount of blood in the ventricles, to decrease significantly. Why? Because the ventricles are contracting, we’re sending the blood out to the body so, that it can go to the muscles, the organs that need blood and oxygen, and all that good stuff. That is the result of the ventricles contracting, so you can see the increase in pressure, the blood being ejected so, you can see the decrease in ventricular volume, and that happens right after the QRS complex which is the depolarization of the ventricles.

So, thus far, we’ve looked at the P wave, atrial depolarization causing atrial systole or atrial contraction. Then, we’ve looked at the QRS complex which then causes ventricular contraction and increase in pressure. Here you have isovolumetric contraction where the valves are close and no blood is exiting the ventricles and then, you have the semilunar valves opening when the pressure in the ventricles can overcome the amount of pressure in the aorta, and that causes ventricular ejection. You can see the term here, ‘ejection’ that means that the blood is being ejected from the ventricles. You can see there’s a significant decrease in ventricular volume.

Then, we have this T wave that represents the repolarization of the ventricles. When the ventricles repolarize, that’s also going to cause the ventricles to relax so, you can see now the amount of pressure in the ventricle is going down significantly. Then, at a certain point, we didn’t talk about this in Episode 51 where we spoke about isovolumetric contraction, the same thing is going to happen on the opposite end where we have isovolumetric relaxation. And, that’s because the valves are closed, the pressure is decreasing, so, you’re going to get a significant drop in pressure while the volume of blood in the ventricle is staying constant. Then, once that’s done, the ventricles are relaxed, the atria are also relaxed the, we can get ventricular filling where blood is being sent back. You can see here during relaxation, this is where the filling happens, blood is coming back from the body, blood is coming back from the lungs and entering the ventricle, so the ventricular volume is going to start going up again, it’s going to increase as you see here, the full thing, increases until we get that P wave again which causes atrial depolarization, and the cycle continues.

Now, there’s one thing we didn’t look at as yet, and that’s the phonocardiogram. You can see here, we have a signal here, a signal here, a third signal here, and there’s actually even a fourth signal. What these represent would be the sounds of the heartbeat. When you listen to the heartbeat, you usually hear a ‘lub-dub’ sound: ‘lub-dub,’ ‘lub-dub,’ ‘lub-dub.’ What that refers to would be the first and the second sound that you see here. Yes, there’s a third sound and there is a fourth sound but, you don’t hear those because they’re not strong sounds. The two main sounds that you hear are the first and the second. What that refers to is the closing of these valves. So, at this point after the QRS complex where the ventricles depolarize and the ventricles start to contract, when they start to contract, that’s going to cause an increase in force closing the valve, closing this atrioventricular valve, and when that valve shuts, you’re going to hear that first sound, the ‘lub’ sound. Then, here, where the ventricles relax after sending all of that blood out, you’re going to get a closing of the semilunar valves and you’re going to hear the second sound which is the ‘dub’ sound. So, you get ‘lub-dub,’ ‘lub-dub,’ ‘lub-dub.’ That is the heartbeat that you hear. This third sound here is when the ventricles are being filled, and as the ventricles are being filled, there’s going to be some turbulence in there and that’s going to cause a third sound but, you don’t hear that as much because there are no valves that are closing or anything of that sort. It’s just blood that’s flowing. The fourth sound that there is represents the filling of the atria with blood. Of course, since the atria are significantly smaller than the ventricles, that sound is going to be even softer. So, you don’t even see it in this phonocardiogram.

This shows the entire cardiac cycle. I hope that now that we’ve gone through all of the details, this entire graph does not look as intimidating as it might have looked when we first started. You can always revisit some of the previous episodes. In Episode 48, we deal with the electrocardiogram, we talk about isovolumetric contraction in Episode 51, and there are a few other episodes covering other details involved in this process.

That’s all for this video. Of course, you can visit the website at Interactive-Biology.com for more Biology videos and other resources. That’s it for now, and I’ll see you on the next one.

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Isovolumetric contraction is that stage when the ventricles continue to contract even though the blood volume stays the same. How and when exactly do this happen?

Watch to learn more.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 51, I am going to talk about isovolumetric contraction. So, let’s get right into it.

What we’re looking at here is diastole at the top and systole at the bottom. So, this is where the ventricles are relaxing and this is where the ventricles are contracting. As you can see, blood is flowing into the atria and then, into the ventricles. Then, when the ventricle contracts, that pushes the blood into the aorta so that, it can go to the rest of the body and also, send blood to the lungs.

There’s something very significant that’s happening here. When the blood comes in, you can see this atrioventricular valve is open to let that blood get in to the ventricle. Once the ventricles contract, that causes this atrioventricular valve to close and of course, the same thing over here, so that the blood does not flow back into the atria.

We see here that this semilunar valve is open. However, that does not happen immediately. When the ventricle contracts, it needs to build up enough pressure to open that valve so that, the blood can flow out of the ventricle and to the rest of the body.

What we’re going to look at over here is what we’ve looked at before where right after the ventricular contraction happens, the cycle starts over and the ventricle fills with blood. So, you’re going to see an increased volume in the ventricle. And then, at a certain point, the atria are going to contract so, when the right atrium contracts, that forces even more blood faster into the ventricle. So, when the left atrium contracts, that forces more blood faster into the left ventricle and then, the ventricle contracts. When it contracts, that is going to push blood out of the ventricle and it’s going to go to the rest of the body. This is the end diastolic volume here and here we have the end systolic volume.

Let’s look at what’s happening in the ventricle when it comes to pressure. During the relaxation period, the diastole, we’re not going to have any pressure in the ventricle. So, we hardly have any so, I’m going to put that around zero. Then, at a certain point, let’s say at this point here, we have the atrium contracting, and when the atrium contracts, that’s going to cause an increase in pressure in the ventricle. Not a huge increase, but, an increase nonetheless. Then, the ventricle is going to contract. When the ventricle contracts, that’s going to cause an increase in pressure in the ventricle.

Let me draw that here. Here, we have that increase in pressure but, as you can see, it’s not until we reach this point that the valve actually opens, the semilunar valve opens, so that the blood can flow out. This is the point that we need to reach. Let’s say that that point is somewhere around 80 mL of mercury so, the pressure has to reach approximately 80. When that happens, the semilunar valves open and the blood gets ejected. We still have some increase in pressure and then, at a certain point, the muscle relaxes, we get diastole, and the pressure comes back down.

This time period, between where the ventricle contracts but the blood does not get ejected, and this point, we call this, (let me do that in a different color), we call this isovolumetric contraction. Why do we call it isovolumetric contraction? “Iso-” refers to the fact that it’s the same; “volumetric ” refers to volume so, the volume stays the same; “contraction” because the ventricle is actually contracting even though the volume is staying the same. The reason the volume is staying the same, is because the valves are closed so, the blood cannot leave until it reaches that point where the semilunar valve opens. Once that opens, the blood can flow out to the rest of the body.

That’s it! That’s the concept of isovolumetric contraction. That is all I want to cover in this episode. As usual, I’d like to invite you to visit the website at Interactive-Biology.com for more Biology videos and the many other resources we’re adding over time. Our goal is to help make Biology fun. That’s it for this video and I’ll see you on the next one.

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Here, Leslie discusses how stroke volume can be regulated. Depending on which factors are changed, blood volume entering the heart may increase and in effect increasing heart contraction too.

Watch, listen, and learn how this happens. Enjoy!

Transcript of Today’s Episode

Hello and welcome to Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 50, I’m going to talk about regulating stroke volume, the skeletal muscle pump and Frank-Starling mechanism. So, let’s get right into it.

So, we’ve been looking at stroke volume and we’ve been looking at the fact that blood enters into the heart, comes in through the atria and then, into the ventricle and then, it gets pumped out, as you can see here, to the aorta, to the rest of the body, and to the lungs, and so on.

Then, we looked at how to determine the stroke volume, and we said, if we have blood entering into the ventricle, the ventricle is being filled and then, at a certain point, the ventricle contracts shooting that blood out to go to the rest of the body and we have the EDV and the ESV, the end diastolic volume and the end systolic volume, the difference between the two, that’s this difference here, that is the stroke volume (SV).

Looking at the stroke volume, if we want to increase or decrease the stroke volume, we can do it in two ways. We can either change the end diastolic volume or the end systolic volume. I guess, you can say we can do it in three ways. We can do one of those two or we can do both of them. If we adjust those, that’s going to change what the stroke volume is.

So, the question today is, how do we change the end diastolic volume and the end systolic volume. Now, I want to look at a number of ways to change the end diastolic volume and the end systolic volume thus changing the systolic volume. But, I’m just going to discuss a few of them so that you can kind of get the concept.

The first where we can do that is by increasing the amount of time that we have before the ventricular contraction. So, if we have more time, we have more time for the ventricles to be filled. So, here it is being filled until about 120 mL. If we increase the amount of time that we have, it might go upto a 140 mL before the ventricles can contract. Then, when the ventricles contract, you can see, we have a greater stroke volume. So, just by increasing the amount of time, that can increase the amount of blood entering into the heart which increases the end diastolic volume and we’re going to show a little later how that even decreases the end systolic volume. So, that’s the first way – by having more space between the heart beats. In other words, by having a lower heart rate.

Another way of increasing the end diastolic volume, let me just write that here, is by causing more blood to be sent back to the heart. How do we do that? Well, there are a number of mechanisms.

The way I want to talk about is called the Skeletal Muscle Pump. What that is, it’s a mechanism for increasing what we call, venous return. The difference between arteries and veins, arteries are the vessels that are going away from the heart and veins are the vessels that are returning to the heart. So, arteries take the blood to the muscles and to the organs and the tissues that need the blood and the oxygen that comes with the blood and once those nutrients and the oxygen are used by the organs and so on, the blood returns to the heart via the veins.

What I’m going to do right now is, I’m going to draw a vein. The cool thing about these veins is that in the veins, we have these valves. So, I’m going to draw these valves. The way these valves are constructed is so that, the blood can only flow in one direction. The blood can enter the veins and go in this direction with no problem. But, if you try to go back in the opposite direction, that won’t work because these valves are actually going to stop them. Now, associated with these veins, we have skeletal muscles. So, this is some skeletal muscle here and this is, I’m just going to draw these strands to show that it’s striated and here, we have more skeletal muscles on this side (Forgive my poor drawing skills). Here we have skeletal muscle on this side and skeletal muscle on this side.

What this does is, it actually contracts in a way that helps to push the blood in the direction that it needs to go. This is something that happens, for example, when you’re exercising, you want more blood going back to the heart so that it can be pumped to the lungs, pick up more oxygen and then be sent back to the rest of the body. So, when you’re working out, you’re exercising, the skeletal muscle pumps are doing their work and they’re helping to push that blood so the blood can go faster, more blood can be going to the heart. That is what we call, increasing venous return. We’re increasing the amount of blood that’s returning to the heart via the veins. There are a number of things that regulate this process. But, this is the concept. Skeletal muscle pump increases the amount of blood returning to the vein. That has to do with increasing the end diastolic volume, the EDV. The other factor that influences stroke volume is the ESV, the end systolic volume.

Let’s look at one of the ways where that is controlled. We’ve looked at muscle contraction and we said that the functional unit of contraction is the sarcomere. This is one sarcomere here. We looked in Episode 041 at how this process happens. When muscle contraction happens, we have this that we call, myosin. This is the myosin filament. The blue here, we call actin. This is “A” for actin and this is “M” for myosin. On the myosin we have myosin heads and those myosin heads associate with the actin and they pull so that, this process can happen where we have the sliding filaments. The filaments slide against each other , the muscle contracts and then the muscle relaxes. This is the exact same process that happens in the heart. If you need a review of this process, you can go back to Episode 041 to check out those details.

Now, the way the structure of this sarcomere is set up, in order for us to have the maximum amount of contraction, we have to have optimum overlap. Here, we have the overlapping between the myosin heads and the actin. In order to get the best, the strongest contraction, we have to have maximum overlap.

This is how this works. When the heart gets filled with blood, this stretches out more. So, the end of this sarcomere might be over here because there’s more blood in the heart. That stretching of the muscle causes an increase in contraction for a number of reasons.

Imagine if the end of this actin was over here. There’s an increase distance between these two points so that, it has a farther distance to travel as the sarcomere gets shorter. That’s going to cause a stronger contraction and if you have a stronger contraction, it’s going to send more blood out of the heart, leaving less blood in the heart. In addition to this, we’ve spoken about how calcium is involved in this process. And, you can check out Episode 043 for more details on this. Calcium ions (Ca2+) are released from the sarcoplasmic reticulum. That binds to troponin which is on here, blocking the binding sites for the myosin head. When calcium comes, that exposes the binding site so that the myosin heads can bind freely. The stretching of the heart increases the affinity of this troponin for calcium ions.

If have an increased the affinity for calcium ions, you’re going to have more myosin heads being able to bind to the binding sites on the actin and that is also going to increase the contraction. This is called the Frank-Starling mechanism. It’s called that because it was named after the two guys who first described that process. What it says is that, if the heart gets filled with more blood, that is natuarally going to cause a stronger contraction sending more blood out of the heart and increasing the stroke volume even further by decreasing the end systolic volume. We looked at how this happens. You have better overlap and you have a greater affinity for calcium which is going to cause a stronger contraction.

Once again, if you need to understand the details of how calcium is involved in this process, go back into Episode 043 where I go into those details.
That’s pretty much it for this video. As usual, I want to invite you to visit the website at Interactive-Biology.com for more Biology videos and all of the other resources we’re adding there on a regular basis so that we can help make Biology fun. That’s it for this video , and I’ll see you on the next one.

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Stroke Volume = EDV – ESV

What do these mean? Watch to learn more and understand about stroke volume.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and before I get into this episode, I just want to send a shout out to Richard Morris and his friend, Nathan. Richard sent me an email a few days ago letting me know that they appreciate the videos and that they have watched every single video that I have published here at the Interactive Biology TV. And that is just awesome. Richard and Nathan, I hope you have gotten a tremendous amount of value and, I hope that you continue to get a tremendous amount of value from the videos that you are watching here at Interactive-Biology TV.

I know there are so many of you out there that have been watching the videos and, I want to let you know how much I appreciate every minute that you spend watching these videos. Thank you for every comment that has been left. Thank you for every question that have been asked and all of the feedback that I’ve been getting. It is just tremendous to know that this is helping so many people all over the world. So, thank you, thank you, thank you.

Inside this episode, Episode 49, I’m going to be talking about what is stroke volume and how to calculate it. So, let’s just get right into it.

When I’m talking about stroke volume, I’m talking about the amount of blood that is pumped by one ventricle during each heart beat. So, we know that the heart beats and, we know that blood comes into the heart, and when the ventricle contracts, it pushes that blood out to the rest of the body and to the lungs. We’ve looked at this in detail, in Episode 44. If you need to review that, you can go back to Episode 44 to check out those details.

Here, we’re looking at the heart. Right now, we’re just going to look at the left ventricle. What is happening is blood is coming into the left atrium and then into the left ventricle. When it reaches in the left ventricle, after a short period of time, the ventricles contract and that pushes blood, as you can see here, pushes the blood out into the aorta and that then goes to the rest of the body.

That’s a brief overview but, once again, you can go back to Episode 44 to check out more details about that.
There are a few definitions that I want you to know. Definition number one: systole. Systole is the contraction of the heart. Then we have diastole and that’s the relaxation of the heart. So, systole is contraction, diastole is relaxation then, we have the End Diastolic Volume or the EDV which is the amount of blood in the ventricle right before ventricular contraction. So, right before the ventricle contracts, the amount of blood that we have in the ventricle, we call that the End Diastolic Value which makes sense. It’s right at the end of diastole so, that’s the End Diastolic Volume.

Then, of course we have the End Systolic Volume which is the amount of blood left in the ventricle right after the ventricular contraction. So, when the ventricles contract, and it pushes the blood out to the lungs and out to the rest of the body, the amount of blood we have left over, that is the end systolic volume which, once again, makes sense because its at the end of systole.

With those definitions, let’s look at the graph.

All right. So, what we have here is a graph. On the x-axis we have time and on the y-axis we have volume in milliliters so, we’re looking for the amount of blood in the ventricle.

For this example, we’re going to talk about the left ventricle which is the one that pushes the blood into the aorta to go to the rest of the body.

Let’s say, ventricular contraction has just finished. When that contraction is finished, the ventricles start to get filled with blood again. After that contraction, another cycle starts where blood flows into the ventricle. Here we have blood getting into the ventricle. At a certain point, we’re going to have a more rapid filling, and when it reaches this point, and we’re not going to talk about too many details where this part is concerned. We’re going to talk more about that in a later episode. But, let’s say this is the point where the ventricle contracts. What’s going to happen here is, when the ventricle contracts, that’s going to push the blood out of the ventricle and it’s going to go to the rest of the body.

Here we have a certain amount of blood and here we have a certain amount of blood. The amount of blood that we have in here, right before the contraction, we’re going to call that the EDV. Once the contraction is over, we’re going to call that the ESV.

The way we calculate the stroke value is SV is equal to EDV minus ESD:
SV= EDV – ESD

If the end diastolic volume is 120 mL of blood and the end systolic volume is around, let’s say, it’s 50 mL. The stroke value is going to be 120ml minus 150 mL and that is going to be equal to 70 mL. I just realized here that I wrote 5. I meant to put 50 so, I’m just going to put that 0 here. So 120 minus 50 = 70. Seventy would be my stroke volume.
Again, ventricle fills with blood, the ventricle contracts. At a certain point, the ventricle contracts that pushes the blood out of the ventricle and to the rest of the body. At the end of the contraction, we have an end systolic volume. If the end systolic volume is 50 mL and the end diastolic volume is 120 mL, the stroke volume will be 120 minus 50 and that is going to be equal to seventy.

That’s pretty much it for this episode. Of course, if you want to see more, you can go to Interactive-Biology.com where we have more Biology videos and many other resources. We’re adding to the resources on a regular basis to try to help make Biology fun. That’s it for this video and I’ll see you on the next one.

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Have you seen an ECG reading? What do those lines mean? How does it measure heart activity?

Watch and learn as Leslie once again teaches us about this topic.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 48, I’m going to show you how to read an electrocardiogram. For short, it’s called ECG or EKG. So, let’s get right into it.

First, I want to answer the question, what is an electrocardiogram? An electrocardiogram is a test that records the electrical activity of the heart. We looked at how the  SA node starts the signal and we looked at how that signal spreads to the rest of the heart. You can always go back to Episode 46 for more details on how that works.

The ECG is used to test for irregularities in how the heart functions. You’ve probably either seen this first hand in a hospital or on TV. You can look at the electrocardiogram and it will tell you if the heart is working the way it should. The way this is conducted is by placing skin electrodes on different parts of the body. These electrodes are able to detect the electrical activity of the heart. When you look at the electrocardiogram, it looks kind of like this {Leslie shows an animation of an electrocardiogram} and you’ve probably seen this. Normally when you see this, there’s a beep associated with it. There’s no beep in this animation but, you get the point.

What we’re going to do is we’re going to look at this and we’re going to look at each component of the electrocardiogram. Let’s look at it right now.

We’re looking at an electrocardiogram and you can see that we have a number of things. We have this peak over here. We’re going to call this the P wave, this peak right here. And then, we have this section that we’re going to call the QRS complex. Then, we have the T wave and sometimes we get this U wave. We’re going to talk about what these different waves show.

The P wave. We’ve looked at how the SA node generates the signal and then that signal spreads to the muscle cells in the atria. What this P wave shows us is the depolarization of the atria. Okay, so, when the atria depolarizes, we see this peak.

We have the QRS complex, you probably guessed it by now but, this shows the depolarization of the ventricles. That is what is represented by the QRS complex.

Then, we have the T-wave which comes after the QRS complex and this shows the repolarization of the ventricles.
Now, you’re probably wondering why the signals that come from the ventricles are significantly larger than this little signal that comes from the atria. But, if you look at the heart, you’ll see that the atria is significantly smaller than the ventricles. So, when the cells in the ventricles depolarize, that’s going to have a much greater effect on the EKG or the ECG because you have more cells depolarizing so you can get a stronger signal. And then of course, you get the repolarization.

The U wave is one that you don’t always see. It’s sometimes hard to see and in most cases, you don’t really see it. But, in some cases, you do see it. In some cases it can tell you something about when things are going wrong with the heart. We’re not going to go into all those details but, I included it here because it was shown in this pictures that I found and because it does show up sometimes. Some people think it’s the repolarization of the Purkinje fibers. And it’s also thought to be the repolarization of some other specialized muscle cells. But, we’re not going to go into that.

The main things are the P wave, the QRS complex and the T wave. The P wave being the depolarization of the atria; the QRS complex being the depolarization of the ventricles and; the T wave being the repolarization of the ventricles.

If you ever need a refresher on what the terms depolarization and repolarization mean, you can always go back and to Episodes 9 and 10 and that will give you more details.

Well, that’s all for this video. As usual, I’d like to invite you to check out the website at Interactive-Biology.com for more Biology videos and other resources to help make Biology fun.

This is Leslie Samuel. That’s it for this video and I’ll see you on the next one.

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Leslie explains how action potentials are generated by the cardiac cells of the heart and how the release of calcium can generate heart contraction.

Watch to learn more.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where were making Biology fun. My name is Leslie Samuel and in this episode, Episode 47, I’m going to be talking about action potentials and contraction in cardiac muscle cells. So, let’s get right into it.

I’m looking at the heart. We’ve looked at a number of things related to the heart. In the previous episode, we spoke about the SA node, which is what we see here, number one and, we spoke about the AV node, which is this part here, number two, and we spoke about these Purkinje fibers. I’m just going to write PF for now. So, this is the AV node, the SA node and the Purkinje fibers. You can go back to the previous episode to learn more about those, in case you’re not sure what they do; in case you’re not sure how they function.

There are a number of things that I want you to know here. We said that the SA node functions as the pacemaker. There’s an important feature about the heart muscle cells that you need to be aware of. That is the fact that these cells are all electrically connected. So, all of the muscle cells in the ventricle are electrically connected, all of the muscle cells in the atria are also electrically connected.

What that means is that if one of the cells in the ventricle gets stimulated, that signal is going to travel to all of the other cells in the ventricle. Not only that, but, if the SA node starts a signal, that signal is going to spread. This is why we get the heart contracting in response to the signal that’s generated by the SA node. Then, when it reaches the AV node and it spreads via the Purkinje fibers, that signal spreads to all of the muscle cells in the ventricles, causing the ventricles to contract.

There are some other important details that you need to know. When the signal is generated in the SA node and it spreads to the atria, the conduction velocity is one meter per second (1 m/s). So, the signal spreads at a speed of 1 m/s here. At the AV node, it slows down to where it’s somewhere around 0.04m/s. Then, in the Purkinje fibers, it speeds up significantly, and we get a conduction velocity of 5 m/s.

So, what this means is that we have a signal that starts here and spreads throughout the atria relatively quickly at 1 m/s but then, it slows down at the atrioventricular node to 0.04 m/s. So, there’s a delay here, and then, after it passes the atrioventricular node, that signal spreads rapidly to the ventricles. Now, why do we want this? As we mentioned before, the blood first goes to the atria and then, the atria contracts, sending the blood from the atria to the ventricles.

You don’t want the atria and the ventricles contracting at the same time. That would cause problems. You want the ventricles to get filled with the blood from the atria first and then, you want the ventricles to contract sending all that blood to the rest of the body and to the lungs. So, that’s how that works and that is why it’s good that we have this slowing down at the atrioventricular node.

Now that we know that and now that we understand that the muscle cells are all connected electrically, let’s move on and look at what happens inside the muscle cells.

We have a stimulus that comes from the AV node or the SA node and that spreads to the muscle cells. In response to that, what’s going to happen is that the membrane potential of the cardiac muscle cells is all of a sudden going to depolarize very quickly. So, we have that initial depolarization. When the muscle cells depolarize, as with skeletal muscles, we’re going to have calcium being released from the sarcoplasmic reticulum. For a refresher of how that works, you can go back to Episode 42 where I talked about calcium release and how that causes muscle contraction.

Once the calcium is released from the sarcoplasmic reticulum, that’s going to prevent the repolarization that normally happens rather quickly. With a normal neuron, the action potential lasts less than a millisecond. However, in cardiac muscle cells, we have calcium that’s being released that slows down the repolarization process and we get a phase that’s referred to as the ‘plateau.’ The membrane potential does not repolarize as quickly. Then, at a certain point, calcium gets pumped back into the sarcoplasmic reticulum, potassium also leaves as usual, and we get the repolarization of the cardiac muscle cells.

As you can see, the time scale that we have here shows that this action potential can last as much as 300 milliseconds as opposed to the one millisecond or less than one millisecond that we get with a neuron. That’s because of the calcium released. That’s because of this plateau phase.

Let’s see what that does for muscle contraction. Yes, we’re going to have a depolarization but then, we’re going to have the calcium released and that is going to cause the muscle cells to contract just like I showed in Episode 42. Once again, you can always go back at Episode 42 to revisit that concept.

This is what we’re going to do. I’m going to plot the tension in the cardiac muscle cells. So, we’re looking at the cardiac muscle and here, nothing is happening. But, as soon as calcium starts being released, that’s going to cause the muscle cells to contract. This is what’s going to happen. This is the tension and then, once calcium starts being pumped back into the sarcoplasmic reticulum, the muscle cell is going to relax and go back to its resting state.

So, we have the action potential lasting significantly longer than we’ve seen before, because of the calcium that’s released from the sarcoplasmic reticulum and that calcium then causes the muscle cells to contract and we get this tension in the muscle cells.

As the calcium gets pumped back into the sarcoplasmic reticulum and the potassium ions leave, that is going to cause the muscle cells to relax and go back to its original state.

And that’s pretty much it. The action potential causes calcium release. Calcium release causes muscle contraction.

That’s all I’m going to cover in this video. As usual, you can head back to the website at Interactive-Biology.com for more Biology videos and for more resources that we’re adding there on a regular basis. So, stay tuned. This is Leslie Samuel. That’s it for this video and I’ll see you on the next one.

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In this episode, Leslie discusses the effect of adrenaline and acetylcholine on heart rate. These two modifies the conductance of the ions across the membranes of the cells of the SA node causing either an increase or a decrease in heart rate.

Watch and learn how it all works.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 46, I’m going to talk about how adrenaline and acetylcholine affect heart rate. So, let’s get right into it.

In the last episode, Episode 45, we looked at this slide where I showed that in the SA node, we have a pacemaker potential that results in a spontaneous signal so that we have the heart beating in response to these action potentials that are automatically generated in the SA node.

If you haven’t looked at Episode 45, I would recommend for you to pause this right now and go and watch Episode 45 so that you’re going to get a full understanding of what we’re going to be talking about.

Let’s go to the next slide. I’m sure you’ve all been in situations where, let’s say you’re doing something and someone jumps up behind you and scares you. What happens? Your heart starts beating faster. The reason it starts beating faster is because adrenaline is released from the adrenal gland that’s located above the kidneys. When that adrenaline is released, that causes the conductance in the pacemaker cells to change. As you can see here, we have an increased conductance for sodium and calcium ions. That is going to cause those to rush into the cell much faster.

It’s going to look a little different than what we looked at before because the membrane potential is going to increase significantly faster so that we’re going to get a faster action potential. So, it might look something like this. As you can see, the signal happens much faster. Forgive my sloppy drawing here. So, we have signals being produced much faster and the heart rate increases. If you remember from the last one that I showed, I was able to show two action potentials on this. But, because sodium and calcium ions are rushing in much faster, the signals are going to be generated much faster because it’s going to reach the threshold much faster and we get an increased heart rate. So, that’s adrenaline.

Now, there’s an opposite effect where instead of adrenaline being released, we have acetylcholine being released. I didn’t plan for the acetylcholine to come in as a flame but, it did for some reason.

What happens when acetylcholine is released? As you can see up here, the conductance for potassium is going to increase significantly. You should know that potassium wants to leave the cell. So, this is going to increase hyperpolarization and is going to slow down depolarization.

What’s going to happen is, instead of this rapid depolarization, we’re going to get a significantly slower depolarization so that, it takes much longer to reach the threshold. When it reaches the threshold, the usual process happens: voltage-gated calcium channels open and calcium rushes in to the cell. Then, we have our depolarization. Then, this process continues.

But, as you can see here, depolarization is much slower than over here. Here, depolarization is sped up because sodium and calcium are rushing into the cell much faster in response to adrenaline. Here, it’s going to be much slower because more potassium is leaving the cell causing depolarization to slow down and we get a slower heart rate.

Faster heart rate in response to adrenaline; slower heart rate in response to acetylcholine.

That’s pretty much it for this video. As usual, you can visit the website at Interactive-Biology.com for more Biology videos and all of the other resources we’re putting together over there. This is Leslie Samuel. That’s it for this video and I’ll see you on the next one.

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In this episode, Leslie talks about how a pacemaker potential can cause a heart to beat automatically. Details about how it is generated is discussed in this video. Just how does this happen, our heart beating again and again?

Watch to learn more.

Have fun and enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 45, I’m going to be talking about the pacemaker potential of the S.A. node and the A.V. node. We’re basically going to look at how this results in the heart beating automatically. So, let’s get right into it.

Let’s first talk about the S.A. node. The S.A. node stands for the sinoatrial node and you can see it in this figure over here, it is number one. That’s this cluster of cells. It is basically a specialized group of cardiac muscle cells that don’t contract which is kind of strange. They’re muscle cells and they don’t actually contract. But, what’s special about these cells is that they are adapted to automatically generate impulses. So, it can automatically cause signals that can spread throughout the heart, causing the heart to beat. The S.A. node functions as the pacemaker of the heart. Yes, we have the A.V. node and some other stuff that we are going to talk about but, these generates signals faster than any of the others so, it sets the pace for the heartbeat. As you can see, it is located in the right atrium.

So, now let’s talk about the A.V. node. The A.V. node is number two. So, it’s this cluster of cells here and it stands for the atrioventricular node. It is similar in function to the S.A. node in that it automatically generates impulses and it is located between the atria and the ventricles hence the name, atrioventricular node.

Let’s go back to the S.A. node and see how this results in the pacemaker potential. Before we look at that, I just want to point out that we have, in addition to the S.A. node and the A.V. node, we have some fibers that extend from the A.V. node and spread throughout the ventricle and those fibers are called Purkinje fibers. These are also very important in that they spread that signal throughout the rest of the ventricle.

Let’s talk about the S.A node. We said that that functions as a pacemaker. So, we are going to look at the pacemaker cells that we have in the S.A. node. What is special about these cells is that normally, there’s a significantly higher conductance for sodium than there is for potassium. Now, if you go back to Episode 006, I talk about Donnan equilibrium and driving force and I show how there’s normally a driving force for sodium to rush into the cell. I also show that potassium wants to leave the cell. Because the cell is much more permeable to sodium, we’re going to have a situation where there’s much more sodium coming in than potassium leaving.

Because we have more positives going in than leaving, what we’re going to get is a pacemaker potential where the cell normally depolarizes. Then, when it reaches the threshold, something interesting happens. Yes, we have the sodium rushing in and some potassium leaving but, now that we’ve reached the threshold, voltage-gated calcium channels open and calcium is going to rush into the cell. So, we’re going to get this rapid depolarization. In other words, we’re going to get an action potential.

At the peak, we’re going to get a different situation where, yes, we have sodium coming in and potassium leaving but, voltage-gated potassium channels are going to open so that the conductance for potassium increases significantly and potassium is going to rush out of the cell repolarizing the membrane.

At that point, we still have the sodium that’s coming in and the voltage-gated potassium channels close so, we have the initial situation where sodium is rushing into the cell, causing this depolarization then, the same thing happens. It reaches the threshold, voltage-gated calcium channels open depolarizing the cell membrane once again, causing that impulse. Voltage-gated potassium channels open causing potassium to rush out of the cell again. This process continues over and over and over. What ends up happening is we have this automatic signal that’s generated constantly resulting in the contraction of the heart. This causes the heart to beat.

It’s really that straightforward but, the main idea is that the cells in the S.A. node have a significantly higher conductance for sodium so it continuously depolarizes causing that impulse that causes the heart to beat.

That’s really all I want to talk about in this video. As usual, you can visit the website at Interactive-Biology.com for more Biology videos and other resources to help make Biology fun. This is Leslie Samuel. That’s it for this video and I’ll see you on the next one.

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How does the blood move around the body? What is the role of the heart in bringing blood to all the different parts of the body?

Watch and see as Leslie gives an overview of the Circulatory System, the first in this series.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 44, I am going to be talking about how blood flows through the heart. This is going to be the first video in the Circulatory System series. So, let’s get right into it.

Here, we are looking at two pictures of the heart. On your left, we’re looking at the heart when it’s being filled with blood. On the right, we’re looking at the heart when it’s pumping the blood out of the heart. We’re going to look at a number of details here just to give an overview of how the blood flows through the heart. In order to understand how the blood flows through the heart, we need to look at the valves that are found in the different parts of the heart.

First of all, allow me to point out that this is the right side of the heart so, this is right. Over here, we have the left side of the heart. Now, that looks a little strange because when you’re looking at the screen, this is your left and this is your right. But, this is looking at it as an individual that’s facing you. This would be his right side and this would be the left side.

There are a number of valves that are found throughout the heart. There are a number of parts of the heart that we need to know.

The first thing I want to point out is here, we have the right atrium and the left atrium. So, this chamber is the left atrium. This chamber is the right atrium. Then, we have the right ventricle and the left ventricle. Same thing over here, we have the right ventricle, left ventricle; right atrium and left atrium.

The next thing I want to point out is that between the atria and the ventricles, we have what we call the atrioventricular valve. And that makes sense since it’s between the atria and the ventricle. So, here we have an atrioventricular valve, here we have an atrioventricular valve. Now, on the right side, we also call this atrioventricular valve a tricuspid valve. We call it “tricuspid” because it has three cusps, in other words, three flaps. You’re only seeing two here but, that’s because this is a cross-section. Then, on the left side, we have what we call the left atrioventricular valve which is also known as the mitral valve or the bicuspid valve. I’m just giving you these different names so that if you go and read a textbook and it says one of these, you know exactly what it’s talking about. So, we have the tricuspid or the right atrioventricular valve and the bicuspid or the mitral or the left atrioventricular valve.

Then, we have valves that allow blood to leave the ventricles. On the right side, we have the right semilunar valve and that is also called the pulmonary valve. The reason it’s called a pulmonary valve is because it leads into the pulmonary artery. On the left, we have this semilunar valve which we can also call the aortic valve. We call it the aortic valve because it leads into the aorta.

So, these are the different names and I want you to know these names: tricuspid, bicuspid, mitral, atrioventricular, aortic, semilunar, which is the pulmonary and the aortic. Those are the valves that I want you to be familiar with.

The special thing about valves is that it allows for blood to flow in one direction. So, here you can see blood can flow into the ventricle but, it can’t flow back. If it tries to flow back, these valves are going to shut. So, all of these valves are one-way valves. They allow for blood to flow in one direction.

Now that we know the different valves, let’s look at how blood flow happens. Blood comes back from the body and it enters into the heart via the vena cava. So, you can see blood is flowing into the vena cava. We have the posterior vena cava and we have the anterior vena cava. Blood is coming in, entering into the right atrium.

As it enters into the right atrium, the atrium contracts and that pushes the blood into the right ventricle. Once the blood gets into the right ventricle, the ventricle contracts and that pushes the blood through the semilunar valve or the pulmonary valve into the pulmonary artery. And from here, that blood goes to the lungs. And, it goes also in this direction to the lungs.

Once the blood goes to the lungs, it picks up, you guessed it, oxygen because you’re breathing in the oxygen. That oxygen aids the blood. Once the blood gets oxygen aided, it leaves the lungs and goes via the pulmonary veins into the left atrium. The left atrium contracts sending the blood through the left atrioventricular valve into the left ventricle. Once the blood is in the left ventricle, the left ventricle contracts and that sends the blood through the semilunar valve or the aortic valve in this case, into the aorta, and then, that blood can go to the rest of the body.

I know this looks a little confusing with all of these arrows but, let’s follow that one more time. Blood comes from the body. It enters via the posterior and anterior vena cava into the right atrium. The right atrium contracts and that pushes the blood through the tricuspid valve or the right atrioventricular valve into the ventricle. The ventricle contracts and that pushes the blood via the semilunar valve or the pulmonary valve to the pulmonary arteries that go to the lungs, picks up oxygen, then it comes back oxygenated via the pulmonary veins into the left atrium. The left atrium contracts and that pushes the blood into the left ventricle. The ventricle contracts, pushing the blood via the aortic valve or the semilunar valve to the aorta and out to the rest of the body.

So, the function of the heart is basically to pump the blood to the body, to send the blood to the lungs to pick up oxygen, and then to send that oxygenated blood to the muscles and to the organs that need it. Once the muscles and the organs that need it, once they use that oxygen, the blood comes back via the vena cava to the heart. The process can continue over and over again.

I have these two over here and you can see, this shows the heart filling with blood and, this shows when the ventricles actually contract and send the blood out to the lungs and to the rest of the body via the aorta.

There’s one thing I’d like to emphasize though. I say that, first the right atrium contracts and then the right ventricle contracts, and I’m saying that just because I’m showing it one at a time. But, both atria contracts simultaneously and both ventricles contract simultaneously. So, that while this process is happening, this process is also happening. Blood is being pumped to the lungs. At the same time, it’s being pumped to the rest of the body.

That gives you a general introduction into the circulatory system by showing you how the heart pumps blood.

As usual, you can visit the website at Interactive-Biology.com for more Biology videos and other resources. That’s all for this video, my name is Leslie Samuel and I’ll see you on the next one.

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Join Leslie as he shares this last video on muscle contraction explaining with full clarity the smallest details on how this works.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 43, I am going to go into the details of muscle contraction. This is going to be the last video in the muscle contraction series, so, enjoy! Let’s get right into it.

You can always go back to Episode 42 to refresh your memory but, we said that the functional unit of contraction is called the sarcomere and, that is what we’re looking at right now. This unit is one sarcomere. We said that we have a thick filament that is called myosin and, we have a thin filament that is called actin. We said that, when muscle contraction happens, the more the neuron releases neurotransmitter that stimulates calcium release. When that happens, the fibers slide against each other just like this. So, as the muscle fibers becomes shorter, that is the muscle contracting. And you can clearly see that in this animation.

The reason we said that this can happen is because on the myosin filaments, we have these heads and those heads extend and bind to the actin. When they bind, they kind of flex so, it moves in this direction and that pulls the actin shortening the sarcomere.

What we are going to do today is we’re going to look at the details of what is happening there. We are going to look at six steps in muscle contraction. This is another image that’s showing something similar to what we’ve looked at. We have the myosin heads. Let me do that in a different color so that you can make sure to see it because we have a lot of red there. We have the myosin heads that are binding to the actin filaments.

Here, we are going to be looking at that in more details. We have the actin. Yes, it’s a different spelling because it’s from a different language but, on the actin filaments, there are two things that are very important. We have tropomyosin as you see here so that’s this long strand here. On top of the tropomyosin, we have troponin. This is a complex that we find all along the actin filaments.

Here’s the situation. Because this is here, the myosin heads want to bind to the actin. There’s some binding sites on the actin so, let’s say this is a binding site right here. But, what’s the problem? The tropomyosin is covering that binding site so, the myosin heads cannot bind. Okay, so, we have these myosin head-binding sites all along the actin; myosin heads want to bind, we have all these myosin heads ready to do their business but, they cannot because it’s blocked by the tropomyosin.

All right so, let’s go now and look at the six steps of muscle contraction. Step number one. Calcium is released from the terminal cisternae. Remember we said that the terminal cisternae is a part of the sarcoplasmic reticulum and that is where calcium is stored. So, calcium is released. You can see here, we have this little binding site for the calcium so the calcium now comes and binds the troponin. So, here we have calcium and binding to the troponin. And then, what that does is it causes a conformational change. To put it more simply, we’re just moving the tropomyosin-troponin complex. So, that moves and, when that moves, it exposes the binding sites on the actin. That’s step number one. So, step number one: We had calcium in the terminal cisternae that is released when there’s a stimulus. The calcium ions bind to the troponin causing a conformational change in the troponin-tropomyosin complex. In other words, it’s moving out of the way. And then, the next step can happen. That step is, the myosin heads can bind to the binding sites on the actin. So, this is the one binding site. For simplification we’re just showing one myosin head but, as you know we have many myosin heads all along this actin.

In order for that to happen, we said that there’s normally ATP that’s on the myosin heads and you saw that, you saw that in the previous figure. But, that ATP has to be hydrolyzed to become ADP and an inorganic phosphate (Pi). So, we have ADP and the phosphate. All right, so, we have the myosin head that has bound to the binding site on the actin. That was step number two. Step number three. This ADP and Pi is released from the myosin head. I’m not showing that in the figure but, just imagine that being released. When that is released it causes the power stroke. In other words, it causes this guy here to flex. And when it flexes, it moves in this direction and that causes the actin to slide across the myosin.

Okay, so, calcium is released, step number one, binds to the troponin, causes this change in the troponin-tropomyosin complex so that it gets out of the way; ATP being hydrolyzed into ADP and inorganic phosphate is a state that this needs to be in for the myosin head to bind. When those are released, the myosin head flexes and we get the power stroke. That’s step number three.

Let’s go to step number four. Step number four is another one that I’m not showing but, we have ATP. So, this is an ATP molecule that comes in and binds to the myosin head. When that binds to the myosin head, the myosin head then detaches from the actin so, we no longer have that connection. That’s step number four.

Step number five. ATP is hydrolyzed which re-energizes the myosin head. So, once we have ATP being hydrolyzed like it is here, that re-energizes the myosin head and it’s ready to go again.

One more step, step number six. This calcium here needs to be gone. So, we have the terminal cisternae and it’s not shown here. So, I’m just going to draw it with my great artistic skills. We have calcium pumps in the terminal cisternae. What that does is it basically pumps that calcium back in. So, we have calcium being pumped back in that is going to cause the troponin-tropomyosin complex to go back to where it was and it’s going to be blocking… I should have done that in green to keep the consistency. Oh, I still can, why not. Okay, so we have the troponin-tropomyosin complex that is blocking once again the binding site for the myosin head.

All right, so let’s recap on that real quick. Step number one: Calcium is released, binds to the troponin. When it binds, it causes a conformational change or a shift, whichever one you want to call it, it causes that shift exposing the binding sites on the actin. Step number two: Myosin head binds to the actin. Remember that the ATP has to be hydrolyzed into ADP and Pi in order for that to take place, it has to be re-energized. It gets that from that hydrolysis process. Step number three: ADP and Pi release that causes power strokes that causes this guy to flex. Then, ATP comes in, binds to the myosin head, causes the myosin head to be released from the actin. The myosin head gets re-energized when the ATP is hydrolyzed back into ADP and Pi. Calcium ions are pumped back into the terminal cisternae and this process can happen again.

Well, that’s pretty much it. That is muscle contraction. If you have any questions, go ahead and leave them in the comments. That’s all for this video, and I’ll see you on the next one.

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Now that you have an overview as to how muscle contraction works, here Leslie now discusses in more detail how it is affected in the presence of calcium. What really happens when these ions are released?

Watch to learn more and enjoy!

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 42, I am going to talk about how the release of calcium ions results in muscle contraction. So, let’s get right into it.

So, here we’re looking at a muscle and there are a few terms that I want you to know. This is called the fascicle, so this section right here, that’s a fascicle and that is basically a bundle of muscle cells. And, this of course then would be individual muscle cells or, as I said in the last episode, you can also call it muscle fibers. What I’m going to do now, is we’re going to take this muscle cell and we’re going to look at it much larger here. Here you can see we have the muscle cell, the muscle fiber and that is made up of these individual myofibrils. So, this would be a myofibril.

We looked at the myofibril in the previous episode and we showed how they’re made up of sarcomeres and I’m going to call a sarcomere from right here, you see this part here, to here, that is one sarcomere. As I said in the previous episode, this is the functional unit of contraction. We’re going to look at how calcium ions is responsible for the contraction of this sarcomere. And, we’re going to look at an animation of how that contraction looks.

So, let’s go to the next slide. Here, we’re looking at the sarcomere and we looked at the parts of the sarcomere. We said that we had a thick filament and that thick filament was myosin, and then we had a thin filament, and that thin filament is called actin.

Now, when muscle contraction happens, it’s because of the sarcomere becoming shorter, this is moving in and I’m going to animate that for you. This is contraction happening, and then the muscle relaxes and it goes back to how it was before. Contraction happens, the muscle relaxes, and then it goes back to how it was before. To put that in perspective, this is me working out in the gym, and as I contract the muscles in my arms, this is what happens. So, my bicep muscles contract, I pull it up, you can see it shortening. The sarcomere is getting shorter. We looked a little bit at how that happens. We said that there are myosin heads on the myosin that actually pulls along and pulls the actin so that this entire unit gets shorter. As the sarcomeres get shorter, and you have many of them along the myofibrils, as they get shorter, the muscle contracts and that causes my lower arm to move up in that direction.

So, now let’s take that and look at a little more detail. So, we’re going back to this picture where we’re looking at the muscle fiber so, that’s this part here again, and as we look at the muscle fiber, there’s something that I want you to notice. Here, we have the membrane that surrounds the muscle fiber and that membrane, we’re going to call that the sarcolemma. Now, you’re probably noticing that I’m using this prefix sarco- a lot. That prefix sarco- refers to the muscle. So, the sarcolemma, the sarcomere… anytime you hear sarco-, you can assume that we’re talking about something relating to muscle. The interesting thing about the sarcolemma is that you have these little openings where the membrane actually goes deep into the cell. And you can see it coming here and you can see it going through there. Where the membrane goes deep into the cell, that is called T-tubules. So, they’re basically these little tubes that go deep into the cell. And they serve a very important purpose. This is how it works.

Last time we looked at the fact that axons come in and make synaptic connections with the muscle cells. This is called the neuromuscular junction. So, when a signal comes down, and it releases the neurotransmitter, in this case the neurotransmitter is acetylcholine, and releases that neurotransmitter, it binds to the receptors that causes the signal in the muscle cell membrane, in the sarcolemma. That signal then travels deep into the cell via these T-tubules and something very important happens. Now, you can see that it looks like it’s one tube that’s going down deep into the cell. But, that tube, I’m going to take that and draw it over here and it’s not by itself. So, here we have the T-tubule and then surrounding the T-tubules, next to the T-tubules, we have the sarcoplasmic reticulum. So, I’m going to draw those here and it’s just going to look like tubes coming down next to the T-tubule. It’s not shown here but, I’m going to show that over here. And, as I said that is called the sarcoplasmic reticulum. The sarcoplasmic reticulum stores calcium ions. So, we have calcium ions inside the sarcoplasmic reticulum. So, let me illustrate that here so, Ca2+, Ca2+, and that’s all throughout the sarcoplasmic reticulum, it’s being stored there for when it needs to be used.

So, once again, we have a signal that’s coming down the axon causing a signal in the sarcolemma. That signal then goes deep into the muscle via the T-tubules. On the T-tubules, we have a receptor that we call the dihydropyridine receptor and on the sarcoplasmic reticulum, we have a receptor that we call the ryanodine receptor. So, let me write those over here. The red is the dihydropyridine receptor (hopefully, I‘m spelling this right) and here we have in blue, the ryanodine receptor. All right, so we have our signal, the signal comes along the sarcolemma, that signal spreads deep into the muscle cell via the T-tubules, that’s going to cause the dihydropyridine receptor to interact with the ryanodine receptor, that it opens the channel and let calcium ions flow out into the cell. Okay so, calcium is flowing out into the cell, out of the sarcoplasmic reticulum, and when that calcium flows out, that then causes muscle contraction. I’m not going to go through all the details as to how it causes muscle contraction in this video but, I’m going to do that in the next episode.

The take-home message is, the signal comes via the axon, causes a signal in the sarcolemma, that signal travels deep into the muscle cell via the T-tubles. Because of the relationship between the dihydropyridine receptor and the ryanodine receptor, that causes calcium that is stored in the sarcoplasmic reticulum to be released, and the calcium released then causes muscle contraction. So, we can look at it here again and we can see here, this is where calcium is being released, and then the calcium is then pumped back out, calcium is being released, calcium is pumped back out.

Now, there’s one thing I didn’t mention and that’s the second part with calcium being pumped back out. You have the T-tubule, you have the sarcoplasmic reticulum, and in the membrane of the sarcoplasmic reticulum, you also have calcium pumps and once the signal is over, the calcium pumps pump the calcium right back into the sarcoplasmic reticulum. So, that’s what’s happening here, calcium being released, calcium being pumped back in, calcium being released, calcium being pumped back in.

That’s all the content for this video. If you have any questions, of course you can ask them in the comments section below, and as usual, you can visit the website at interactive-biology.com for more Biology videos and other resources. That’s it for this video and I’ll see you on the next one.

http://www.youtube.com/watch?v=UDvEm9DbXc0

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Ever wonder how our muscles contract and what makes them do so?
In this video, Leslie gives a clear overview of how muscle contraction works.

Enjoy!

Transcript of Today’s Episode

{Video begins with Leslie in a gym doing some sets of bicep curls} Oh, hey! Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 41, I’m going to give you an introduction to skeletal muscle contraction. But, one second. Let me finish my set. {Leslie goes back to finish a few more sets of his bicep curls.}

So, here I am working out in the gym and I am doing some bicep curls. I’m lifting the weight and there’s muscle contraction happening. Now, when I’m talking about skeletal muscle, I’m talking about this voluntary muscle. The muscle that I have control over and it’s the ones that I use to move my bones, to move my body, to walk, to lift weights, and as you can see here, I am doing some bicep curls. I am using my biceps.

Now, let’s look over here to the right. You will see that the biceps are these muscles over here. And, what I’m actually doing is I’m contracting these muscles, making these muscle fibers shorter, and as they become shorter, they are actually pulling my arm up in that direction. So, I’m making these muscles shorter by contracting them and that is pulling on the bones in my arms, my lower arms and that is raising my lower arms.

Now, you can see here that there are a lot of stripes. We call these stripes, striations. And, each individual fiber that you see here is one muscle cell. So, these cells are narrow but, they are also very long. So, these are the muscle cells and you can see they are many muscle cells that make up each muscle and each muscle group.

Now, what we are going to do is we are going to take one of these muscle fibers and look at what’s happening there. So, let’s go to the next slide.

Here we have one muscle fiber and, you can see we have an axon coming in. So, the axon here is number one and that axon makes a synaptic connection with this muscle cell or another thing you can call it is a muscle fiber. And the interesting thing about this muscle fiber is that it’s made up of these tubes that kind of go all the way along, kind of like little fibers inside the muscle fiber and those are called myofibrils. So, we have the muscle fiber or the muscle cell which can be very long and very slender and narrow. We have the axon that is coming in making a synaptic connection with the muscle cell and these little fibrils, myofibrils inside of the muscle cell. This entire thing with the neuron, the motor neuron and the muscle cell, this is called a neuromuscular junction. In other words, it’s the junction or the connection between the nervous system and the muscle cells.

Now, what I’m going to do is I’m going to take one of these myofibrils, these guys in here and I am going to look at that down here. So, let’s go ahead and do that. And, this is going to look a little strange but, what I’m basically doing, this is one fiber. All of these here, it actually extends much longer than that. This is looking at one of these fibers. And you’re going to see that there are these different sections, and it goes from here to here, and then, from here to here. We’re going to talk about what these different components are and what role they play in muscle contraction.

Now, right here, each one of these units, I call a sarcomere. The sarcomere, this important unit here is the functional unit of contraction. This is really where the contraction happens. The sarcomere is made up of two main fibers. The main fibers are actin, and this narrow one here, I’m going to call actin; and the thicker fiber is called myosin. So, we have actin filaments and myosin filaments. So, we have actin and we have myosin.

And what’s happening as I contract my muscles is that on the myosin we actually have these little heads that extend and, you know what I’m just going to zoom in on one of those heads and you can see that over here. We have the myosin head here and it’s connecting to the actin and what that does when contraction is supposed to happen, this actually moves and pulls against the actin. So, you can imagine here. You have these little heads that are pulling, pulling in this direction, and what ends up happening is, this distance here shortens as this moves in and this moves in because of the heads that are pulling on it.

So, once again up here you have the myosin head that’s moving in this direction. As it moves in that direction, it pulls the actin along, and that pulling shortens the sarcomere so that you might have maybe the sarcomere being this long instead of that long. So, it’s shortening it. And, what that’s going to do, it doesn’t only happen here, it happens here, it happens here, it happens here all along the muscle fiber or the muscle cell, that shortens the muscle and that causes contraction.

All right so, we’re just kind of going over the major details that are happening. In future episodes, we are actually going to look at these individual steps and break them down a little more. But, for right now, that’s just an introduction into muscle contraction, specifically, skeletal muscle contraction.

That’s it for this video. If you have any questions, you can leave them in the comments and you can always visit the website at interactive-biology.com for more Biology videos and other resources. That’s it for now, and I’ll see you on the next one.

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Do you ever wonder what happens to the hair cells inside our ears as we hear sound? What role do these tiny hairs have in hearing?

Watch this short movie as Leslie explains clearly and vividly enough for us to understand the main role of these tiny hair cells as sound enters our ears.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun!  My name is Leslie Samuel and in this episode, Episode 40, I’m going to talk about the role of hair cells in hearing. So, let’s get right into it.

In Episode 39, we looked inside the cochlea to see what happened in response to sound. What we said was, in response to sound, the basilar membrane vibrated up and down, and this is the basilar membrane, which causes the Organ of Corti, which is this section here, to vibrate up and down, causing the tectorial membrane to move in a windshield wiper-like fashion that causes these hair cells to bend, the stereocilia, and the hair cells bend, causing a signal in the auditory nerve that then goes to the brain.  The brain says, “Okay that is sound,” and you hear it.

What we’re going to do today is we’re going to look specifically at what happens inside these hair cells, specially the inner hair cells which are directly responsible for the signal being sent to the brain that results in the sound that you are hearing.

So, let’s look at what happens inside those hair cells.  All right, so, I’m going to draw a hair cell.  Let’s say this is my hair cell right here. On the hair cell, I have stereocilia.  Now, this stereocilia occur in pairs: we have a long one and a short one.  In the short one, we have potassium channels so, that’s the potassium channel right here.   But, what’s interesting is that the long hair cell is mechanically connected to the short hair cell via that gate. Now, as you can imagine, when the tectorial membrane moves down on this hair cell, that causes the hair cell to bend.  So, let’s say this hair cell, the long hair cell, bends in that direction.  What is that going to do to these channels?  That’s going to cause these channels to open.  Now, these channels are mechanically-gated potassium channels.  They’re not extremely selective to potassium but, for this purpose, we’re going to look at what it does with the potassium ions.

Now, in the fluid that’s surrounding these stereocilia, we have endolymph. An endolymph is very rich in potassium ions.  So, let’s say we have potassium ions, K+, all around here.  When these mechanically-gated channels open, that is going to cause potassium ions to flow into the hair cells.  What is that going to do to the membrane potential (Em) ?  That is going to increase the membrane potential. Once the membrane potential increases, something else happens.  We have calcium ions that are also outside the cell. When that membrane potential increases, potassium is in here that’s going to cause calcium channels, voltage-gated calcium channels to open and calcium is going to rush into the cell.

Now, if you can remember when we spoke about neurotransmitter release, we said that calcium ions are the trigger that causes the neurotransmitter release in axon terminals.  This is the exact same thing that happens.  We have neurotransmitters in vesicles here and those neurotransmitters are then going to be released, and as I showed in the previous picture, this is connected to the auditory nerve, and that sends signals to the brain.

That’s all the content for this video.  I hope you learned a lot.  If you have any questions, go ahead and leave them in the comments below. That’s it for now, and I’ll see you in the next one.

http://www.youtube.com/watch?v=fSO6i5qNWG0

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The organ of corti – such a small part of the cochlea with such a major function. Watch as Leslie demonstrates how the vibrations in the cochlea affect the cilia on the hair cells, and how this process is translated to hearing.

There’s also a really cool video of a hair cell dancing to Rock Music.

Enjoy!

Transcript of Today’s Episode

Hello, and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel and in this episode, Episode 39, I’m going to be talking about the function of the Organ of Corti. And don’t worry, I won’t be singing in this episode. That’s Episode 38. So, if you want to hear me sing, go to Episode 38 and enjoy! Today, we are just going to talk about the function of the Organ of Corti. So let’s get right into it!

Now, we’ve been looking at this picture and we’ve been looking at the structure of the ear. We look at the fact that sound waves come in here; cause vibration in the tympanic membrane; causing the malleus, incus, and stapes to vibrate; and then causing the fluid inside of the cochlea to vibrate. In the last episode, we unrolled the cochlea and we looked at it like this. And we showed that, depending on where it vibrates, that’s going to send signals to the brain, and the brain can interpret that as a certain pitch, a certain frequency.

Now, there are a few things that I want you to pay attention to in this episode that we did not pay attention to in the previous episodes. And that would be here. We have the scala vestibuli. That’s this cavity at the top here. And below the basilar membrane, we have the scala tympani. And that’s the cavity at the bottom of the cochlea, beneath the basilar membrane.

And what I’m going to do in the next picture is, I’m going to actually take a cross-section. So I’m going to cut straight through the cochlea like this, and we are going to look at a cross- section of the cochlea. So let’s go to the next figure.

Here, we are looking at the cross-section of the cochlea. And here, you can see we have the scala vestibuli. And here we have the scala tympani. And here, this is the basilar membrane. And right above the basilar membrane, we have the Organ of Corti. So that’s this section right here. We can’t see too many details about it, but that is the Organ of Corti. Here we can see more details. This entire structure is the Organ of Corti.

But I just want you to pay attention to how it is laid out here, with the Organ of Corti here, scala vestibuli at the top. This is the basilar membrane. And here we have the scala tympani. One more place that I want you to pay attention to, here, is another cavity we call the cochlear duct. And once again, in here we have the Organ of Corti. So this is a cross-section of the cochlea, and that’s how it’s laid out.

Now, I want to bring your attention to the Organ of Corti which is shown clearly right here. Once again, we can see here we have the basilar membrane, and on top of that we have the Organ of Corti. A few more things to point out here. This membrane here, it says membrana tectoria. We call this the tectorial membrane.

And we look at the fact that, when sound enters the cochlea, that causes the basilar membrane to vibrate up-and-down. Now, when that vibrates up-and-down, that’s going to cause the Organ of Corti to move up and down. Then, here we have the tectorial membrane that’s attached only at one end. So, as the basilar membrane is going up-and-down and the Organ of Corti is going up-and-down, that is going to cause the tectorial membrane to move in a windshield- wiper-like fashion. So it’s just going to flap like a windshield wiper.

Now, in the Organ of Corti, we have a number of different hair cells. We have inner hair cells, which would be this one here; and we have outer hair cells, which would be these four here. Now, as you can imagine, if the entire Organ of Corti is moving up-and-down, the tectorial membrane is moving in a windshield-wiper-like fashion, that tectorial membrane is going to cause this outer part of the hair cells to vibrate. And these outer parts are called cilia. So, it’s going to cause the cilia to bend. And that’s the process that’s going to cause a signal to go via the auditory nerve to the brain.

Now, there is a very important thing to understand here. The part that responds to the tectorial membrane that is directly responsible for hearing would be the inner hair cells. And that sends a signal to the brain. However, the outer hair cells are involved in modulating the response and helping the inner hair cells so that you can hear better.

So once again, when the sound comes into the cochlea, the basilar membrane vibrates up-and-down that causes the tectorial membrane to move in a windshield-wiper-like fashion, causing the cilia and the hair cells to bend. And when the cilia and the inner hair cells bend, that causes a signal to be sent to the brain. The outer hair cells are involved in modulating the response to that sound.

Now, I have a very fascinating video to show you that’s going to show what happens to the outer hair cells in response to sound. So sit back, relax, and enjoy the ride!

{Short Video Clip of Outer Hair cell dancing to music}

So, as you can see in a very interesting way, this hair cell was vibrating up-and-down. It was vibrating in response to the sound. And that process is involved in modulating the response to hearing. This causes signals to be sent to the brain and the brain gets a full picture of the sound that you are listening to.

That’s it for this video. If you have any questions, as usual, leave them in the comments section below. And you can always visit the website at Interactive-Biology.com for more Biology videos and other resources. That’s it for now, and I’ll see you in the next one.

http://www.youtube.com/watch?v=Id-LO_7e9BI

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Some people sing high, others sing low. There are so many pitches, which are the result of different sound wave frequencies.

How does the ear allow you to distinguish between these various pitches? Watch this video and listen as Leslie details the processes in the inner ear that result in us being able to tell the difference.

Enjoy!

Transcript of this Episode

“Aaa! Aaa!  Aaa! Aaa!” (high tone to a deep tone) Hello! Welcome to another episode of Interactive Biology TV where we’re making Biology fun. My name is Leslie Samuels and I apologize for what you had to listen to at the beginning of this episode. In this episode, episode 38, I’m going to talk about how we hear different pitches. And what do mean by different pitches? I’m glad you asked. I mean, “Aaa! Aaa! Aaa!” (high to low pitch).

I’m sorry, I apologize. I shouldn’t be putting you through that. But, that is exactly what we’re going to be talking about today. I just made a few different sounds and they were different pitches. We want to look at how your brain is able to distinguish the different pitches based on what is happening inside the ear. So, “Let’s continue,” (high pitch). “Let‘s continue.” (Low pitch).

Here we’re looking at the ear. We’ve looked at this figure in the last episode and we looked at one that was similar to it in the episode before that. Where we ended off last time, we had a signal coming in, and we spoke about how the malleus, incus, and stapes are involved in transferring that signal to the cochlea. What I’m going to do now is, I’m going to take this cochlea and I’m gong to roll it out and just kind of extend it.

So, we’re not going to look at it like how it looks here, kind of like a snail. We’re going to look at it as if was just rolled out. So, let’s go to the next picture.

Here we have it. We have the cochlea that we unrolled and now it extends right here. What you’ll see is, here we have a membrane that we call the basilar membrane, and here’s the writing for that right here. This is the basilar membrane. What you’re going to notice about the basilar membrane is it’s thinner over here than it is over here.

So, at this end, it’s significantly thinner and as it goes away from the oval window where the malleus, incus, and stapes connect, as it goes away from that section, it gets thicker and thicker and thicker until it’s thickest right here at this end.

What you’re going to see here is, we have a number of frequencies that are associated with these different sections. Here we have at 25 Hz which is a low frequency, and as we come over to the thinner section, we have higher frequencies up here to 1600 Hz. And, it goes all the way up here to about 20 kHz. So, we go as low as 25Hz and as high as 20kHz.

If you’ve taken a Physics class, you know that higher pitches are the result of higher frequencies. Forgive my writing there again. So, higher pitches are the result of higher frequencies and lower pitches are a result of lower frequencies. And, we’re talking about the sound waves, the frequency of the sound wave.

If a certain sound comes into the ear, causes the tympanic membrane to vibrate, the malleus, incus, and stapes vibrate, and that causes the oval window to vibrate, that’s going to cause fluid inside the cochlea to vibrate. Now, depending on the frequency, it’s going to cause a different section of the basilar membrane to vibrate.

Is it easier to move a thinner piece of membrane or a thicker piece of membrane? The answer to that question should be quite obvious. It’s much easier to move a thinner piece of membrane than it is to move a thicker piece of membrane. So, in order for it to vibrate down here, we need more force. You’re going to get a greater force from lower frequencies. Just think about it, if you’re in front of a huge speaker, I mean, massive speaker, and there is sound coming out of that speaker, you’re playing some music, and you’re playing music that has a lot of frequencies. For example, something like this – {nice high frequency music played}.

Now, if you’re standing in front of that huge speaker that’s playing that nice little soft high-frequency music, it’s not going to have a huge effect on you. But, if you start playing something with a lot of bass, something like this – {Music played with lots of bass}.

That’s going to cause you to move. You might even feel the wind of the speaker vibrating and causing the ear to be pushed. You might actually feel that. That’s because when you have lower frequencies, the lower the frequencies, the greater the force that comes along with that frequency.

So, here, in order to cause this to vibrate, we’re going to have a lower frequency sound, which makes sense. That’s why we’re showing 25 Hz here. The closer up we go, where we have the thinner membrane, we can cause that to vibrate with a higher frequency tone. If the frequency is low enough, that might actually cause this entire basilar membrane to vibrate.

The take home message is, depending on the frequency, we’re going to get different regions of the basilar membrane vibrating. This then sends a signal to the brain. Depending on where that signal is coming from, if that signal comes from here and it goes to the brain, that is going to tell the brain that it’s coming from a low frequency and, the brain is going to interpret that as a lower pitch.

If it’s coming from over here, it’s going to the brain, and that’s going to tell the brain that it’s coming from this region which is associated with a higher frequency, and the brain is going to interpret that as a higher pitch.

So, there’s a direct relationship between where it vibrates and where in the brain is being stimulated and depending on where it’s stimulated and where the signal comes from, the brain is going to be able to distinguish between the different pitches. Now, you’re hearing me speak and me speaking right now is a result of a number of different frequencies combining together.

So, there is going to be a complex interaction here, different parts of them is going to be vibrating in different ways, and the brain is going to take all of that and paint the picture of the sound that’s coming from my voice, well, that’s coming from the speakers that you’re listening to this video on and, you can easily distinguish between my, “haa!” (high pitch) and my, “haa!” (low pitch).

I hope that wasn’t too painful and I hope it makes sense. That’s really all for this video. If you have any questions, go ahead and leave them in the comments below. And of course, you can always visit the website at, www.Interactive-Biology.com for more Biology videos and other resources. That’s it for this video and I’ll see you on the next one!

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In this episode, Leslie talks about how sound is transferred to the inner ear. Because there is fluid inside the cochlea, impedance matching has to take place for the vibration in the fluid to accurately represent the sound that you are hearing.

Watch this video to learn how this process works.

Transcript of Today’s Episode

Hello, and welcome to another episode of Interactive Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, episode 37, I’m going to talk about how sound is transferred to the inner ear.

Let’s see and visit an animation that we looked at in the last episode. We looked at this animation that showed how, when you hear something, there are sound waves that are entering into the ear, and those sound waves come in contact with the eardrum, the tympanic membrane.

The tympanic membrane vibrates back and forth and that vibration is transferred to the three bony ossicles, the malleus, incus, and stapes. It’s connected to the cochlea, and that’s going to cause something to happen in the cochlea that’s going to cause a signal to go via the auditory nerve to the brain. That is how we hear.

Now, what we’re going to talk about is what happens in the process of moving that sound, transferring that sound to the inner ear. Later on, we’re going to look at what happens inside the cochlea.

So, let’s get into some more detail. Here, we’re looking at a structure of the ear. We have the outer ear, so, I’m going to refer to this part, up until the tympanic membrane or the eardrum as the outer ear. Then, we have this section here with the malleus, incus, and stapes, the Eustachian tube. This is called the middle ear (forgive my writing there).

Then we have the with cochlea, the semicircular canals, and the nerves and so on, that’s called the inner ear. We’re going to be talking about the process of sound being transferred from the outer and middle ear to the inner ear.

Now, here’s the deal, in the external auditory canal, that’s in here, we have air. In the Eustachian tube that’s in here, we have air once again. However, inside the cochlea, we don’t have air. We actually have fluid. Now, because of that, it’s going to be harder to get the fluid inside the cochlea to vibrate than it is to get the air inside the middle ear and inside the outer ear to vibrate. Think about it this way. if you’re running in air, which, when you’re running you’re usually running in air, that is not as hard as if you’re trying to run in water.

So, in order for us to have the same strength of signal out here and in the fluid inside the cochlea, something needs to happen and that process is called impedance matching. Impedance is basically resistance and we’re trying to match the amount of resistance here to the amount of resistance here. We want the same signal in the fluid in the cochlea that we have in the air inside the outer ear.

This can sound a little confusing because sometimes, I’m referring to “air,” and sometimes I’m referring to the “ear.” But, what we’re basically saying is, when the signal comes here and causes the tympanic membrane to vibrate, we want the signal to be transferred with the same amount of strength to that fluid inside the cochlea. So, we have to go through this process of impedance matching.

There are two ways that impedance matching is accomplished. Let’s look at the first way. Here we have the three bony ossicles, the malleus, the incus, and the stapes that‘s attached to the oval window here. Now, I’m going to draw the malleus, incus, and stapes over here in a very simple way. So, let’s say this is the malleus, this is the incus and, this is the stapes. Now, it makes sense that if the malleus vibrates back and forth, so let’s say it’s going back and forth, that’s going to cause the incus to vibrate back and forth, and then that’s going to cause the stapes also to vibrate back and forth.

However, because of the way these are connected and the hinges that we have between these three bones, I’m not necessarily going to get the same amount of movement here as I get here. I can orchestrate this in a way that when this moves, these are connected so that these will move even more than this is moving. It will move a greater distance. And this is exactly how the malleus, incus, and stapes are set up so that we have a movement ratio of 1.3 to 1. In other words, and I’m going to take a random number, if this moves 1 micrometer back and forth, this is going to move 1.3 micrometers back and forth.

So, we’re going to get more movement here than we are getting here. And that is going to cause increased pressure on the oval window. So, we’re going to have a certain amount of pressure here, but the amount of pressure we get on that oval window is going to be greater. This is exactly what you want because you want to move the fluid inside the cochlea the same amount, you want the same amount of vibration that we have inside the tympanic membrane so that you can send an accurate signal to the brain via the cochlear nerve, or another name for this is the auditory nerve. So, the first way to compensate for the fact that we have fluid in here is by having a movement ratio of 1.3 to 1 between the stapes and the malleus. That is the first way.

Now, let’s talk about the second way. Here, once again, we have the tympanic membrane or the eardrum, and here, we have the oval window. Now, you will notice something about the size of the two. The tympanic membrane is larger than the oval window. To be more specific, it’s approximately 18.6 times larger. Now, why is this significant? I’m glad you asked. Let’s take a very graphic example. Let’s say we have a surface here and we’re going to see that that surface is your leg. On top of that leg, we’re going to put a block, let’s say we have a brick. What happens if someone comes along and decides they want to punch that brick with a certain amount of force. They punch that brick, it’s on top of your leg, and you might say, “Ow!” because it might hurt. I hope that makes sense.

Now, let’s take a different situation where once again, we have your leg but, instead of having a brick, we have, brace yourselves, a needle! I know what you’re thinking already. This is kind of crazy. Well, it is! Let’s say a person comes by, and they do the same exact thing. They come by and they punch that needle that’s right on the surface of your leg. This is the same amount of force that they punch over here. Are you going to notice the difference in the amount of pressure? I am betting that you will! This is going to hurt much more. Most likely if they’re punching, the needle is going to go into your leg and you are going to scream.

I don’t care how strong you are, you are going to scream. The same amount of force as here however, here you have an increased amount of pressure because you have a smaller area. So, I’m going to write here, “smaller area.” This is not the situation that you want to find yourself in. However, in some cases, it can be a good thing. Here, where we have the tympanic membrane being 18.6 times larger than the oval window, what that is going to do is cause an increased amount of pressure due to this vibration. And, what’s that going to do? Well, we said, we have fluid inside the cochlea, air inside the Eustachian tube and inside the outer ear and we want to match the vibration out here which is easy, with the vibration in here which is harder because of the fluid.

So, once again, the two ways that impedance matching is accomplished so that we can get an accurate amount of vibration inside the cochlea is by having a ratio of 1.3 to 1 between the malleus and the stapes; and by having the tympanic membrane 18.6 times larger than the oval window. That’s going to cause the fluid inside the cochlea to vibrate in a way that matches the vibration that’s happening out here. Then, that causes a signal that goes via the auditory nerve to the brain.

In the next video, I’m going to talk more about what happens inside the cochlea. So, make sure to check that one out. That’s it for this video. If you have any questions, as usual, feel free to ask them in the comments section below and I’ll be happy to respond to your questions. Who knows? I might even make a video to answer your specific question. Also, you can always visit the website at Interactive-Biology.com for more Biology videos and other resources. That’s it for now. I’ll see you on the next one.

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 In this episode, Leslie talks about how we hear sounds. From the external ear to the eardrum, down to the 3 bony ossicles, then to the cochlea to be sent as signals towards the brain, it is all explained in this video.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 36, I’m going to be giving an overview of the mechanism of hearing. Now, you’re listening to this video right now, well you’re watching this video right now, and you’re hearing the words that I’m saying that have been recorded. What we’re going to do is look at how that process happens. So let’s get right into it.

We’re looking at a drawing of the ear, and there are a few things that I want to point out here. Here we can see that this is the external part, so this is the external ear. Then we have this section here, and that is called, I’m going to draw a line down here, that’s called the external auditory canal. Then here, there’s a structure that we call the eardrum. Connected to the eardrum, we have 3 small bones. We call them the 3 bony ossicles: the malleus, the incus, and the stapes. Depending on which book you read, you’ll see malleus, incus, and stapes, or hammer, anvil, and stirrup. They all mean the same thing. This is the hammer, this is the anvil, and this is the stirrup. I’m going to be using malleus, incus, and stapes. The way I typically remember this is MIS, mis: malleus, incus, and stapes. Those are the 3 bones. One here, one there, and this is the third one here.

Then we have this structure here that looks kind of like a snail, and that is called the cochlea. Then we have, let me do this in a different color, we have this structure here, and that is the auditory, of course, because it deals with hearing, the auditory nerve. That, of course, goes to the brain. So these are the parts that I want you to pay attention to. Once again, we have the external ear, and in some places, you’re going to see this called the pinna. Then we have the external auditory canal, we have the eardrum, malleus, incus, and stapes, the cochlea, and the auditory nerve.

There are a few other things that we have, like these are called the semicircular canals. I’m not going to talk about that much today. And then we have this connection here where the stapes connects to the cochlea, and that’s called the oval window. And then there’s the round window on the other end of the cochlea. So these are the parts that I want you to know. Now we’re going to talk about how hearing happens. We’re going to give an overview of the mechanism of hearing.

Now, sound exists as waves. You have particles in the ear that are vibrating back and forth, and there’s kind of like an oscillation. That is how the sound starts. Something vibrates, causing the ear to vibrate, and what you’re hearing is a result of this process. So the sound waves are coming from some source, let’s say you’re listening to this right now, which you are. We have sound waves that are coming from the speakers. The speakers are vibrating back and forth. The external ear focuses those sound waves into the external auditory canal. The air molecules are vibrating back and forth, and that vibration comes and strikes the eardrum. When the sound waves strike the eardrum, the eardrum is going to vibrate back and forth. The malleus, incus, and stapes are connected to the eardrum. The malleus is connected to the eardrum directly, the incus is connected to the malleus, and the stapes is connected to the incus. So that causes those bones to vibrate.

When those bones vibrate, it’s going to cause the oval window to vibrate. In the cochlea, which is what it’s connected to, we have fluid inside that cochlea. When the oval window vibrates, the fluid inside the cochlea is going to vibrate, and that’s going to cause a series of vibrations. We’re going to look at what’s going on in here in more detail in the next episode, but the vibration in here is going to cause a signal in the auditory nerve, and that signal then travels to the brain.

So we have the same general mechanism when it comes to senses. There are receptors inside of this cochlea that’s going to respond to the vibrating fluids. That’s going to cause a receptor potential that is going to cause a signal to be sent to the brain, and then the brain is going to interpret that signal. In this case, it’s going to interpret it as sound, and you’re going to hear what I’m saying or you’re going to hear something that you’re listening to. Whatever is the source of that sound, you will be able to hear it because the brain is interpreting what is happening with the receptors that are found inside the cochlea.

There’s one more term I’d like to point out, and that is the eardrum. Another name for the eardrum is also the tympanic membrane. So if you ever hear me referring to tympanic membrane, that is exactly the same thing as the eardrum.

I have an animation to show you that depicts this entire process, and you can see that here. There are a few things I want to point out. You can see the sound waves coming in here, and then you can see the vibrating eardrum. Then you can see the bones, the 3 bony ossicles: malleus, incus, and stapes. Those are vibrating, causing stuff to happen in the cochlea. Of course, I’m being a little vague there, but we’re going to get into more detail in the next episode. In response to these sensory receptors detecting that vibration, that’s going to cause a signal in the auditory nerve that goes to the brain.

So there you have it. You can see the entire process happening. This, of course, is just an animation, but it gives you a good overview of how hearing takes place. If you have any questions, of course you can leave them in the comments section below, and I’ll be happy to answer your questions. You can always visit us at www.Interactive-Biology.com for more biology videos and other resources to help make biology fun. That’s it for this video, and I’ll see you in the next one.

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In this episode, Leslie tells us about on center, off surround ganglion cells. See how the configuration of rods with respect to the ganglion cell’s receptive field influences the type of response we get when those rods are stimulated.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 35, I’m going to talk about a specific type of ganglion cell that we call “on center, off surround ganglion cells.” Let’s get right into it.

I have a ledger over here that shows to the top left that R stands for rods, B stands for bipolar cell, H stands for horizontal cell, and G stands for ganglion cells. Here, I’m starting with a ganglion cell. We’ve look at the way rods connect to ganglion cells via bipolar cells, so I’m going to show that right now. So here we have 4 rods, and you can see those 4 rods here. Those 4 rods are making synapses with bipolar cells, and the bipolar cells are connecting to this ganglion cell. So this ganglion cell connects to 2 bipolar cells that connect to a total of 4 rods.

When we have this configuration with the rod directly connected to a bipolar cell that is directly connected to a ganglion cell, we call this the center of that ganglion cell’s receptive field. So this is the center of the receptive field, so any stimulation that results in activity in these rod cells is considered to be in the center of that ganglion cell’s receptive field.

Then we can have another configuration where we have rods that are connected to bipolar cells, so here we have a rod that’s connected to a bipolar cell that’s connected to a horizontal cell, and then it connects to the ganglion cell. So it goes via a bipolar cell, then a horizontal cell, and that eventually gets connected to this ganglion cell. Since it’s not directly from the bipolar to the ganglion cell, like it is over here, we call this not the center, but the surround. So any stimulation that stimulates these rods is considered to be in the surround of that ganglion cell’s receptive field.

So once again, these rods are considered to be in the center of this ganglion cell’s receptive field because they are connected directly via a bipolar cell to that ganglion cell. These rods, these two, the one over here and the one over here to the left are considered to be in the surround of that ganglion cell’s receptive field because they don’t go directly from the bipolar cell to the ganglion cell. They go via a horizontal cell.

Now, if this ganglion cell is considered to be an on center, off surround ganglion cell, that’s going to give a specific type of response. This is the response. I’m going to draw a graph over here that plots, as usual, the membrane potential versus time, and I’m going to draw one over here that does the same thing, time and membrane potential. We’re going to say that this is the center, this is when rods in the center of the receptive field are stimulated, and this is in the surround. We’re going to get 2 different responses. The response that I’m going to get here when there’s stimulation from the center is that we’re going to get an increase in the membrane potential, so it’s going to depolarize, and as we looked at with the ganglion cells before, we’re going to get a burst of nerve impulses in response to that stimulus. This is the on center response.

Now, if a rod gets stimulated in the surround of that ganglion cell’s receptive field, we’re going to get the exact opposite where we’re going to get a hyperpolarization, and then the membrane potential is going to come back up. In some cases, what we’re going to get here once this hyperpolarization happens and we get this rebound back to where the membrane potential was before, you’re going to get a burst of nerve impulses, but those nerve impulses are going to come after the stimulation. This is called a post-inhibitory rebound. So that’s basically saying it’s post-inhibition, so it’s after that inhibition happens, we’re going to get a rebound and some firing as soon as the stimulation stops.

Once again here, in the on center response, we get depolarization and a burst of nerve impulses in the ganglion cell. In the surround, we’re going to get an off surround response which is basically going to give us hyperpolarization, and then a post-inhibitory rebound. And you can see that those are 2 totally different responses, and the key ingredient here in that off surround response are these horizontal cells, because when they get stimulated by these bipolar cells, they are actually going to inhibit the ganglion cell that you see here. So this refers to the on center, off surround response of ganglion cells. This is a specific type of ganglion cells.

I just want to mention really quickly that we can also have off center, on surround ganglion cells, and if that were the case, we would get an off center response. In other words, if it’s stimulated in the center, we’d get this response over here with the post-inhibitory rebound, and if it’s stimulated in the surround of the ganglion cell’s receptive field, we’re going to get this burst of nerve impulses in response to the depolarization that happens.

That’s really all I want to talk about for this video. If you have any questions, as usual, go ahead and leave them in the comments section below, and I’d be happy to answer your questions. That’s it for now, and I’ll see you in the next video.

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In this video, Leslie explains all about lateral inhibition using two rectangles. Watch to learn how this process helps us see edges of objects more clearly. Enjoy!

Transcript of Today’s Episode

Welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 34, I’m going to talk about how lateral inhibition enhances visual edges. What am I talking about? Well, you’re going to see right now.

Here, we have 2 rectangles. One is darker and the other is lighter. It’s just a solid gray color over here, and a solid darker gray, almost black color, over here. What I’m going to do is I’m going to show you something that’s quite fascinating, at least it’s fascinating to me. It illustrates how visual processing can lead to some interesting things. To a certain extent, it shows that what you see is not always what’s there.

What am I talking about? Well, what I’m going to do is I’m going to take this gray rectangle over here and I’m basically going to move it towards the other one. We’re going to see what happens. Remember it’s a solid gray color, the same color that I have over here, it’s the same color that I have over here, and throughout the entire rectangle. Now let’s put them together and see if anything happens. So I’m just going to move the one on the right towards the one at the left. And now, hopefully you can see this, depending on the monitor that you’re using, you may or may not be able to see this, but I’m guessing you will be able to see it.

What you’re going to notice here is right here at the border, you’re going to see that here is just a little lighter than over here. So before, it looked like a solid gray object, and I really hope you see this, or else this is pointless, and over here now, we’re seeing that it’s darker here than it is over here. If you don’t see it, look closely at the monitor and see if you see a little bit of a lighter edge here.

Now, is that lighter edge there? No, it really isn’t. But there’s something that’s happening inside your eye that’s making it seem as if it’s lighter over here and a little darker over here, you might be able to see that also. So, lighter on this side, and darker on this side, just a little bit. What we’re going to do is look at why that’s the case.

The main idea, though, is that the brain is set up to enhance visual edges so that you can see the edges more clearly. I find this to be very fascinating because to me, it illustrates that maybe what we see might not actually be what is there. And I don’t know how much that extends into everyday life, but it’s an interesting concept nonetheless. Now, let’s look at the cells that we have in the retina.

We looked at this already. We said that here we have the rods and this would be a cone, we said that here we have a horizontal cell, and here we have ganglion cells, and we also have amacrine cells. This is just a review of an earlier episode. The cell that I’m most concerned with now in terms of this process is the horizontal cell. You can see here, we have a number of rods, and we have a cone, and this horizontal cell goes laterally, and it connects to multiple rods and even connects to some of the cones. This is where the processing that enhances those visual edges starts.

So it’s happening in the retina, this entire thing is in the retina. What happens is if it’s getting a lot of intense stimulation from a group of rods over here, that causes this horizontal cell to inhibit some of the other cells so you do not get as much stimulation from those receptors that are not stimulated as intensely as these over here. So we have a strong stimulation coming via these rods or these receptor cells, and that’s causing inhibition of some of the cells that are not being stimulated as much. This process is called lateral inhibition, and to me it’s a very fascinating concept, showing that strong activity over here can inhibit activity in another area.

That’s all I want to cover in this episode. That’s it for this video. If you have any questions or comments, go ahead and leave them below, and I’ll be happy to take a look at them, and maybe even answer the questions that you might have. That’s all for now, and I’ll see you in the next video.

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In this episode, Leslie explains more about the connections between rods and cones to bipolar cells, and between bipolar cells and ganglion cells. He also describes how these connections determine the receptive fields of each ganglion cell. Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 33, I’m going to be talking about the receptive field of a ganglion cell. Let’s get right into it.

In order to understand the concept of the receptive field of a ganglion cell, we need to revisit the structure of the eye. I want to point out that we have this layer of tissue here that we call the retina. In the retina, we have the rods and the cones, and we said that the rods are for black and white vision and just for detecting light, and the cones allow us to see detail, it allows us to see color.

There’s another area, a specific region of the retina that we call the fovea, and this is a very important region because we have a large amount of cones, so much so that we can have up to as many as 150,000 cones per square millimeter. As you can see, that’s a high density of cones. We said that when light comes in, what the lens does is the lens actually focuses that light onto the retina. Specifically, if you’re focusing on an object, it focuses the light onto the fovea, and that allows you to see a lot of detail.

Now, if I am looking directly at my object, and let’s say this is my object here, and you have these photons of light coming off of that object, and that’s being focused onto the fovea. I can see the details of that object. If there’s an object that’s kind of to the periphery, over to the side, so let’s say this is the object over here that I’m not focusing on, that object is also going to be reflecting photons of light, but the photons of light won’t be focused directly onto the fovea. For example, it might be that the photons of light are focused up here.

Now, we still have some pigment here, we still have some rods and cones, not as many as we have in the fovea, so we’re not going to see as much detail, but I can see the object that’s to the left of me right now. I can see that there’s a keyboard to my left, I can see there’s a door to my right. I can’t see all the details of that keyboard and that door, but I can see them.

So, if the light is being focused on the fovea, with such a high amount of cones, a high density of cones, I’ll be able to see more detail. We’re going to look a little bit at some of the processing that happens that makes that possible. Don’t take these arrows as set in stone, I’m just trying to give you a general idea of how this works, but I hope that makes sense.

With that concept, let’s go on now and talk about the receptor field of a ganglion cell. To illustrate that, I’ve simplified the drawing of a ganglion cell, so here we have a ganglion cell, and here we have a cone. So these are all cones, and this is the same for cones or for rods, but we’re going to focus on cones because that really gives us a lot of detailed vision. The cones are connected to bipolar cells, and those bipolar cells are connected to ganglion cells. Here you can see we have one cone that’s connected to the ganglion cell via a bipolar cell. I don’t show that here, but just assume that a bipolar cell is in between here. Here we have another cone that’s connected via a bipolar cell to one ganglion cell. Here we have the same thing.

Over here, we have something a little different. We have 3 cones that are connected to one ganglion cell. Now, from the ganglion cell, we said that the ganglion cells have axons and they send signals to the brain. So, I’m just going to draw an arrow going to the brain from each ganglion cell, and I’m going to draw an arrow going to the brain from this ganglion cell over here also. This is the situation that we have in the fovea. Because we have so many cones, and in some cases, we have one cone that’s connected to a ganglion cell, when the brain is receiving information from these 3 ganglion cells, it’s getting a lot more detail. When it’s getting information from this one ganglion cell that’s kind of trying to summarize all of the information that it’s getting from multiple cones, it’s not going to be as detailed as the situation that we have over here.

So here, the receptive field of this ganglion cell is one individual cone, which gives it a lot of detail. So I’m going to say here, I’m going to say lots of detail. And here, it’s not as much detail. So I can still see what is being picked up by these cones, but I’m not going to see as much detail. So the receptive field of this ganglion cell includes these 3 cones. The receptive field of this ganglion cell just includes one cone. And this can go for cones, it can go for rods, and I draw this simply with 3 cones, but you can get thousands of cones that are connected to one ganglion cell. Of course, that’s not going to give you as much detail, but you’re still going to get some information that can go to the brain and be interpreted so you can see what the objects are with some detail, but not as much.

That’s all I want to talk about in this video. I hope this gives you a good idea of what we mean when we say the receptive field of a ganglion cell, whether you have very detailed receptive field, or not so detailed. This receptive field is larger because it’s connected to more cones, but you get less detail. The receptive field here is smaller, but because you have so many individual ganglion cells that are connected to individual cones and individual rods, that’s going to give you more detail.

If you have any questions about that, you can go ahead and leave them in the comments section below, and I’ll be happy to answer your question. That’s it for this video, and I’ll see you in the next one.

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After the rods and the cones, there are a few other important cells involved in visual processing. In this video, Leslie explains about how the bipolar cells and ganglion cells contribute to this process.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 32, I’m going to be talking about the visual processing that happens in the retina. We’ve spoken a little bit about this in the previous episode, and I want to take this to the next step, the next step in the process.

First, we’re going to start with this animation that’s kind of a review of what we spoke about in Episode 31. There are a few things I’d like to highlight. First of all, if we look here, we have these little round balls, and those are sodium ions. They can be calcium ions also, but for the most part, those are sodium ions. Here we have a channel. In Episode 31, we spoke about this cyclic GMP-gated sodium ion channel. What we said was that if there’s cyclic GMP around, which there normally is in the dark, that channel is going to be open. If that channel is open, as you can see right here, you’ll see sodium is normally able to rush into the cell, and the rod is usually depolarized, and neurotransmitter is being released. So that’s what happens in the dark.

We also have some other things. Here we have phosphodiesterase, as you can see right here. Then we have the trimeric transducin molecule that normally has GDP attached. We have rhodopsin, which is the visual pigment in the rod. And here we have one that we didn’t speak about before, guanylate cyclase, and that’s basically the enzyme that makes the cyclic GMP.

So, in review of what we said before, cyclic GMP is normally around in the dark, depolarization happens. Then, when light comes, we said that a photon of light comes in, and we’ll see that right now, activates the rhodopsin, replaces a GTP, that activates the phosphodiesterase, and when that phosphodiesterase is activated, it converts the cyclic GMP into regular GMP. When that happens, you’ll see here, it closes this gate, and the rod hyperpolarizes. It becomes more negative, it goes toward the membrane potential for potassium.

So there’s a lot of stuff going on in this animation right now and you can see that. My recommendation would be to pause this and go back and look at it again, and kind of try to visualize what’s happening. Look at the details and make sure you understand this, because this is a good overview of what happens inside the rods. As I said in the last episode, the process that happens in the cones is relatively similar to this. So if you get this, you have a good idea of what happens.

So the result of this is, if we’re looking at the membrane potential, or the receptor potential in this case, when the light comes, that is not going to cause the regular action potential. It’s going to cause the membrane potential to go down until that light is gone again, and then it comes back up. This process, as with before with the neuron, this is called hyperpolarization. I’m going to write it as two words because I’m running out of space. Hyperpolarization, so that is what happens in response to light. I hope that review makes sense. If not, go back to the previous episode and you’ll get more of those details.

Now let’s move on and take it from what’s happening inside the rods to what happens with some of the other cells that we have around. So this is looking at the cells in the retina. If light is coming into the eye and it’s hitting the retina, the light is coming in this direction. So it’s coming from up here and it’s going down. There’s an interesting way in which this is arranged in that the rods are actually at the end here. So these are the rods, and here we can see an example of a cone.

There are few other important cells that we need to know about. One would be this red cell here, and that would be a bipolar cell. The next important one that you need to be aware of would be this guy here, these cells here, and those are called ganglion cells. So these are the major players:

1. The rods and the cones
2. The bipolar cells
3. The ganglion cells

You can see here we have some other cells. For example, this one here is called a horizontal cell. We’re not going to focus on the horizontal cells in this video. This is called an amacrine cell. We’re also not going to focus on that in this video, either. So the major ones we’re going to talk about are the rods, and when I say the rods, of course, you can assume that the process is somewhat similar with the cones. We’re going to talk about the bipolar cells, and we are going to talk about the ganglion cells. So let’s look at what happens.

We looked at the process that’s happening inside of the rods before, and we say the net result of that light coming in, so here we have light that’s coming in, and the net result, the overall result, in the rods is that the membrane hyperpolarizes. So here we have a hyperpolarization of the rods. When that happens, neurotransmitter release slows down. It basically shuts off the neurotransmitter release.

Now, the rods are connected, you can see here there are a number of connections, to the bipolar cells. The neurotransmitters that are normally released here are inhibitory, so when it stops releasing those neurotransmitters, it is no longer inhibiting the bipolar cells, and what’s going to happen to the membrane of the bipolar cells is that we’re going to get a depolarization. So it’s basically the exact opposite of this hyperpolarization. Here, we’re going to get in the bipolar cells, we’re going to get depolarization. So let me write here bipolar cells.

Now, bipolar cells, just like rods, don’t have an axon. So this is the entire bipolar cell, but this is not an axon, so we don’t get an action potential. We do get this depolarization, and that is going to cause an increase in neurotransmitter release at these synapses here. So bipolar cells gets depolarized, more neurotransmitter is going to be released, similar to what happens in a regular axon.

Then we have this ganglion cell here, and all of these are ganglion cells. What’s going to happen there in response to more neurotransmitters being released, the ganglion cells are going to also depolarize, but since here we have axons, that’s going to cause a burst of nerve impulses, so a burst of action potentials. These are my spikes, these are my action potentials, these are signals that are travelling along the axons going to the brain.

Let’s look at that again. In response to light, the rod hyperpolarizes, and we looked at the process as to how that happens. That reduces neurotransmitter release, so let me draw here or write here there’s a decrease in neurotransmitter release. Those neurotransmitters are normally inhibiting the bipolar cells. Now, they are no longer being inhibited. They are going to depolarize. That’s going to cause an increase in neurotransmitter release here to the bipolar cells, and that’s going to stimulate the ganglion cells, causing depolarization and a burst of impulses.

So the final result, in terms of what’s happening in the retina, is that these ganglion cells are firing a burst of nerve impulses that are sent to the brain. I hope that makes sense. You can kind of go through that again if anything is unclear so that you can get a better understanding of that.

There’s one more thing I want to talk about. We spoke about the thalamus in the brain, and we said that the thalamus is kind of like the regulatory gateway of the brain. All of the sensory information comes into the thalamus, and then goes to the rest of the brain, or the motor output that’s coming from the brain goes via the thalamus to the rest of the body. There’s no exception here. When the ganglion cells are stimulated and they send their signals, they’re going to send their signals to a specialized region in the thalamus called the lateral geniculate. So this is in the thalamus, and then, that can go on to other parts of the brain for further processing. We’re going to talk about that in some later episodes.

So that’s really it for this episode. Hope everything makes sense. If you have any questions, of course you can ask them in the comments section below, or if you have any comments or anything of that sort, please give me feedback, because I love to get feedback from you guys and be able to help you even better. So that’s it for this video, and I’ll see you in the next one.

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In this video, Leslie explains how rods and cones work, using the rods as an example. Watch to find out how rhodopsin, transducin, and phosphodiesterase, all play a major role in the process of vision.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 31, I’m going to talk about how rods and cones respond to light.

Now let’s do a little bit of a review. We’ve been talking about the eye. We said that in order for us to see something, what happens is light bounces off an object, and in the previous episode, we said that that object was an attractive young lady. So let’s stick with that, and let’s say that light is bouncing off that young lady. It goes through the pupil, and then we have the lens that it goes through. The lens focuses the light onto the retina, and we said especially in the fovea where we have a lot of rods and cones, so that light comes in and it’s focused onto the retina via the lens.

Now, in the retina, as I said, we have rods and cones. These are the receptors that allow us to see. Now what we’re going to do is we’re going to look at what’s happening inside these rods and cones. We’re going to take the rods and use that as an example. However, I want you to know that the process that happens in the rods and the cones are relatively similar. Yes, there are some nuances and differences between the two, but by understanding what happens in the rods, we’re going to also have an idea of what happens in the cones. So let’s look inside the rods right now.

So here we are inside the rods. I know it doesn’t look like it’s inside the rods, but that’s fine. It has the major things that we need. There are 3 main things that I want you to pay attention to. Here we have visual pigment that’s found in the rods, and that’s rhodopsin. Now, rhodopsin is made up of the protein opsin and retinol. The specific form we have this is cis-, it’s a cis-form, so it’s called cis-retinol. Now retinol is basically a slightly processed version of Vitamin A. This explains part of the reason why Vitamin A helps with vision. So here we have cis-retinol and opsin, and together, that makes up rhodopsin.

We also have this molecule over here. It’s a trimeric molecule, meaning it has 3 subunits. This one, this one, and this one. This is called transducin. And then over here, we have this guy here, you see I have PDE, and that basically stands for phosphodiesterase. So these are the major players inside of the rods: rhodopsin, transducin, and phosphodiesterase.

Now, to keep the bigger picture in mind, the phosphodiesterase is the one that really does the damage, and I mean damage in a good way. However, it cannot do what it needs to do because it has these two alpha subunits attached. So these are inactivating alpha subunits. In order for this to do its job, and we’re going to talk about its job in a little while, these alpha subunits need to be removed. Keep that in mind as we go through this process.

So this process all starts with light. We’re going to take one photon of light, and let’s say a photon of light comes in and strikes rhodopsin. So this right here is light, and it comes in and it strikes rhodopsin. When the photon of light strikes rhodopsin, what happens is the cis-retinol changes into a different form, and that different form is called trans-retinol. So it’s no longer in the cis-form, it’s now trans-retinol. When that happens, that causes it to lose its attraction for the opsin molecule, and once that connection breaks, that retinol leaves and what that does is it exposes a binding site on the opsin. That’s what we’re going to use next as we go to the next part of the process.

So what we’ve accomplished so far is we’ve freed up this binding site on the opsin. The next stage in the process involves opsin going over to transducin. Since the binding site is exposed, that can catalyze a reaction. Now, I want you to pay attention here because here, on this subunit of the transducin molecule, you see we have GDP. Once this binding site is exposed, this active site is exposed, that can then catalyze a reaction that converts that GDP into GTP. And you can see here now, we no longer have GDP, we have GTP. So it basically adds a phosphate group on. Instead of GDP, diphosphate, it now becomes triphosphate.

Once that happens, that subunit is activated and that subunit actually leaves the other two subunits behind and goes over to the alpha subunit of the phosphodiesterase. And then, it removes that alpha subunit. So you can see, we said that the goal was to free up this phosphodiesterase. We’re almost there, we have one alpha subunit removed, as you can see here, but we still have one more alpha subunit.

In order to remove this second alpha subunit, this entire process has to happen again, with light coming in, changing the retinol from cis to trans, the retinol leaving, opsin coming over, then opsin comes and catalyzes the reaction to have another GTP, and then we get another subunit. I’m not going to go through the animation of all of this because it’s the same process. But basically here, you can see we have another subunit of the transducin molecule that comes. That can remove this alpha subunit from the phosphodiesterase. So let’s go ahead and remove the second one, and now we have exactly what we wanted, we have this phosphodiesterase and it’s by itself.

I know there are a lot of complicated details in here, but if you keep in mind that this was our goal, it should make sense. So now we have this PDE, this phosphodiesterase, and it can go and do what it does. So what does it do? Well, it converts cyclic GMP into GMP. So it changes this from a cyclic molecule and now it’s just GMP. This is the step that leads to vision. This is how we’re able to detect light.

Now, let’s put this in perspective. We said that we’re inside the rods. And here, I have a picture of a rod, and you can see this is a rod. Here we have a cone, but we’re going to pay attention to the rod since that’s what we’re using as our model. Now normally, with the rod, we have cyclic GMP available. So if there’s no light, there’s no stimulation, there’s cyclic GMP. What that does is it opens up and this is going to sound a little different than what we’ve looked at in the past, but cyclic GMP-gated sodium channels. So this is not a voltage-gated sodium channel, this is a cyclic GMP-gated sodium channel.

So in the dark, we have cyclic GMP around, the cyclic GMP-gated channels, of course, those are going to be open. What’s going to happen is sodium is going to rush in, so we have sodium coming into the cell, Na+. If you remember from previous episodes when we spoke about depolarization, sodium rushes in, making the membrane potential more positive. So this is the exact opposite of what we’ve been looking at because when there’s no stimulation, when there’s no light, cyclic GMP-gated sodium channels are open, sodium is rushing in. As a result of that, the membrane is depolarized and neurotransmitters are being released.

I know what you’re thinking. Why are neurotransmitters being released when there’s no stimulation? It is true, this is exactly opposite to what we’ve looked at, but this is the process and this is how it works in the rods.

Now, once the phosphodiesterase is activated and it gets rid of this cyclic GMP and makes it GMP, what’s going to happen to these channels? These channels are going to close, sodium will no longer rush in, and neurotransmitters will no longer be released. If we were to look at the membrane potential, and since this is a receptor, we’re going to call this the receptor potential. Here we have time, of course, and here we have Em, but in this case, we’re dealing with a receptor potential. Normally, the membrane is depolarized, normally neurotransmitter is being released.

Once this entire process happens and we have GMP instead of cyclic GMP, the channels close, sodium no longer rushes in, and the membrane potential, the receptor potential, is going to go towards the equilibrium potential for potassium ions. So it’s going to become more negative, so it’s going to go down until that stimulation stops, and then it’s going to come back up.

So once again, I want to emphasize that this is exactly opposite because when we get a stimulus, we get a drop in the membrane potential, neurotransmitters are no longer being released, and that’s going to have an effect on the cells that it makes a synaptic connection to.

We’re not going to go beyond this point in this video, but I hope you have a better understanding of what happens in the rods. We’re not going to go into what happens in the cones because it’s a similar process. Yes, there are some differences, but this gives you a general idea. That’s it for this video, and I’ll see you in the next one.

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In this video, Leslie explains all about how we are able to see with our eyes.

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Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 30, I’m going to talk about how eyes work. I’m basically just going to give a little bit of an introduction to how eyes work and how we see, how vision takes place. Before I get into it, I want to give a shout-out to Sarah and the other students in Brain and Behavior at the University of Windsor. They are, right now, going through this content and she sent me a question coincidentally right before I was about to get into this content. So thanks for the questions, and I hope in the next week, I’ll be able to answer those in the videos that I’m going to be doing.

Before I talk about how the eyes work, let’s recap on Episode 29 where we spoke about how senses work. We spoke about the 5 senses, and we said that the general mechanism, the general overview in terms of how it works is: first, receptors are stimulated, then signals get sent to the brain, and then the brain interprets the signals that it’s receiving. This is the way you smell, the way you see, the way you feel and so on. So that’s the general overview. Now, let’s get into the specifics of vision.

Now, imagine this with me. You’re a college student, let’s say you’re a guy and you’re walking on campus, and all of a sudden, out of the corner of your eye, you see a very attractive young lady. She’s so attractive that she causes you to turn your head and take a full look, and you’re just looking at this beautiful lady in admiration. Let’s talk about what happens.

Here we have your eye. This may or may not look like your eye, but it’s going to work for the purposes that I need it for right now. So how this works is there’s got to be light. If there’s no light, you’re not going to see. Let’s say here we have the sun that’s shining, or this light source can be a light bulb, or anything of that sort. But let’s say the sun is shining, and the sun is sending off photons of light. The photons of light are coming in contact with this individual. It’s coming in contact with her hair, with her skin, with her eyes, with all of the parts of her body. As it comes in contact with her body, light is also being reflected, and that light that’s being reflected enters your eyes.

Now let’s look a little closer at this eye. Here we see that we have an opening. That opening is called the pupil. That is a result of what we call the iris, so that’s this section right here, what gives you your eye color. So this iris has pigment that makes the eye appear to be blue. I think this is pigment, at least, I’m not sure if it’s a contact lens or not. But let’s assume this is the natural color of the eye. So the pigment is going to cause it to appear blue.

Now, have you ever noticed that if you go outside and it’s really bright, you end up having to squint? But then after a while, you can see and it’s fine. The reason that happens is because here we have the iris that can dilate. Basically, what can happen is we can adjust the size of this hole. If it’s too bright outside, this will get smaller so that it doesn’t let as much light in. If it’s darker, you come inside a room or anything of that sort, that’s going to expand and the pupil is going to be larger. Now let’s move on from there and see what happens next.

So now we’re looking at your eye, and here you see once again, we have the pupil. Here, you can see iris, and here you can see we have a lens. Now, the cool thing about it is we have also this ciliary muscle here, and that can contract. What that basically does to the lens is it can expand the lens or make it so that you can focus the light onto the retina, and you can see the retina is over here.

So we want to focus on the retina, which is this layer of tissue to the back of the eye, and it goes all the way around. We want to focus the light onto that because in the retina, we have 2 types of pigments, and the pigments are rods and we have cones. You’ve probably heard of these before. The rods are what help us in black and white vision, and the cones help us with color vision. Of course, they work together, but the cones allow us to see color, it allows us to see fine detail. However, the cones aren’t as sensitive to light as the rods. So the rods are really sensitive to light. It doesn’t take much light in order for the rods to be activated, but it does take more in order for the cones to be activated.

You can think about it this way. If you are looking at someone, and let’s say you’re still looking at that young attractive lady and the sun is shining. Now, what happens when the sun goes down? You start to see a little less detail, it gets darker so you can’t see as much detail as you would if there was a lot of light outside. That’s because when you have less light, yes the rods are definitely being stimulated and they’re responding, but the cones need more light in order for you to see bright colors, in order for you to see fine detail. So you lose some detail as it gets darker in the room.

So we have the rods and cones in the retina, and the place where we have the most pigment would be in the fovea. We have especially a lot of cones in this area.

So let’s go back to the scenario we were at before, where you’re looking at this attractive young lady, and light is being reflected off that lady, and it is entering your pupil. It comes in here, it goes through the cornea. It enters your pupil, and it comes to the lens. Okay, I’m going to draw 3 rays of light coming in here.

As I showed you before, the ciliary muscles that are located up here and down here, of course, those can contract and cause the lens to focus the light exactly how you want it to be focused. Now, since we said that we have most of the pigment, especially the cones, we have most of the cones in the fovea, what we want to do then, as this light comes in, you want to contract the ciliary muscles in such a way that the lens focuses the light onto the retina in a way that you can see the details of that attractive young lady.

So the ciliary muscles contract and that causes the lens to then focus the light directly onto the retina, where you have all the rods and the cones, especially in this fovea area where you can see a lot more detail. That is where you want the light to be focused so that you can see that attractive lady, or if you’re reading a book, you want to be able to see the letters and you want to see all the details of the letters. So we want to focus that in the area where we have the maximum amount of cones possible.

Now, we’re going to talk a lot more about what happens inside the rods and cones in a future episode, but right now, I just want to give you a general overview. Light comes in, lens focuses the light onto the retina, then when that happens, that causes a signal in the optic nerve. That signal, of course, goes towards the brain, and as we showed before, the brain then interprets that signal.

Let’s say this process isn’t working very well. Let’s say there’s something wrong with the lens here, where it’s not doing its job at focusing the light onto the retina. What can you do about that? Well, what you can do about that is something that is done very often, somehow compensating for the lens not working well by wearing glasses. So what I’m going to do is, and I’m going to act as if, and forgive my drawing skills here, I’ve never drawn glasses before. But with glasses, what I’m doing is I am putting a lens in front of the eye that can help so that when the light comes in, it gets focused how I want it to be focused, and then I can see the detail that I couldn’t see because of how my lens is compromised.

So there’s going to be a lot of detail in terms of how you create these lenses, and of course, it’s going to vary from individual to individual, but the idea with glasses is we want to make it so that, although the lens that’s inside our eye might not be doing a great job at focusing the light onto the retina in the right way, we can compensate for that by adding an artificial lens and then that can help us out in that process.

That’s really it for this video. It gives us an overview of how vision works and how the eyes work. In a future episode, as I mentioned, we’re going to go in to much more detail, some of the nitty-gritty about how this works even on a molecular level, some of the proteins that are involved and how this really causes a signal in the optic nerve to go to the brain, and what happens specifically in the brain. That’s it for this video, and I’ll see you in the next one.

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In this video, Leslie explains the general mechanism of how senses work.

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Transcript of Today’s Episode

Hello and welcome to another episode on Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 29, I’m going to be giving a general overview of how senses work. So let’s get right into it.

We all know about the 5 senses. We have the sense of taste, smell, touch, hearing, and sight. I’m going to get into some more details, specifically with hearing and sight in future episodes, but for today, I just want to give a framework on which we’re going to base what we’re going to be talking about in the future episodes. So this is how senses work.

We’re going to start with receptors, and these receptors are going to get stimulated. When they are stimulated, they’re going to send signals to the brain. When the brain receives those signals, the brain is going to interpret the signals, and it’s basically going to tell you what the senses are. So if you smell a perfume, it’s because the receptors are stimulated, sending signals to the brain, and the brain interprets that as a beautiful scent or an aromatic scent or however you want to call that. So once again, the receptors get stimulated, signals get sent to the brain, and then the brain interprets those signals.

Let’s look specifically at how this happens in the eye. In the eye, we have the retina. In the retina, we have receptors that we call rods and cones. You can see these receptors right here. When those receptors get stimulated, they’re going to cause a signal that goes via a number of different types of cells, and then it goes via a nerve to the brain. Then the brain is going to interpret that, and you’re going to see the person that’s standing in front of you or whatever it is you’re looking at. You’re going to see that as a result of receptors getting stimulated over here, and then you have a nerve that sends a signal to the brain, and then the brain interprets that signal.

This is the same process for touch. This is the same process for smell and the other senses. Receptors get stimulated, and then that sends signals to the brain, and the brain interprets that signal. That’s really all I want to talk about in this video. It’s not a lot of detail, but trust me, we’re going to start filling in those details in later episodes. We’re going to talk specifically about vision and hearing. That’s it for this video, and I’ll see you in the next one.

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In this video, Leslie explains about the thalamus and the hypothalamus, and the specific functions that they are responsible for.

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Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 28, I’m going to talk about the thalamus and hypothalamus. Let’s get right into it.

Here we have the human brain, and before, we looked at this and we saw that we have the spinal cord that enters the cranium, and as soon as it enters the cranium, we have the brain, which is all of this here. We spoke about the brain stem already, we spoke about the cerebellum, we spoke about the cerebrum. What we’re going to talk about today is the hypothalamus and the thalamus. How I’m going to do that, I’m going to take this area here and show it on a different picture that we can look at in little more detail. So I’m taking that area, and that is what we’re looking at right now.

Here, as you can see, we have this region here that’s called the thalamus, and then right beneath that, we have the hypothalamus. So these are the 2 areas that we’re going to talk about today. What we’re going to do is we’re just going to look at the functions of those 2 areas.

First we have the thalamus, and the thalamus is kind of like a regulatory gateway. The reason I say that is almost all of the sensory input that comes into the brain goes through the thalamus, and the motor output goes via the thalamus to the rest of your body. So it brings stuff into the brain, and this is the gateway that kind of regulates what comes in and what goes out. That’s the function of the thalamus.

The hypothalamus, and if you look at what this really means, “hypo” means under, and “thalamus”, of course that’s the thalamus, so this is right beneath the thalamus. This is involved in functions including homeostasis, emotion, thirst, hunger, circadian rhythms, and control of the autonomic nervous system. The autonomic nervous system involves those processes that you don’t have to think about. Regulating your heart rate and your breathing rate and so on, those are autonomic processes. This is, in some ways, controlled by the hypothalamus.

So there we have it, the thalamus and the hypothalamus. As we go into some of the other things that we’re going to talk about in later episodes, you’re going to see how some of this comes together and we’re going to paint a bigger picture of how the brain and the nervous system works. That’s it for this video, and I’ll see you in the next one.

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In this video, Leslie explains about the different parts of the brain stem and their respective functions.

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Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 27, I’m going to talk about the 3 parts of the brain stem and what their functions are. So let’s get right into it.

Here we’re looking at the human brain, and here we’ll see that we have the spinal cord. The spinal cord enters the skull, and where it enters the cranium, the skull, it then becomes brain. And the first part of the brain that we enter is called the brain stem. The 3 parts of the brain stem are: the medulla, which is this section here; and then we have the pons; and we have the midbrain. So the medulla, pons, and the midbrain, those are the 3 parts of the brain stem.

Now, let’s look at the functions of those 3 parts. First we have the midbrain, and that’s involved in processes such as vision, hearing, eye movement, and body movement. Then, we have the medulla, and that is involved in maintaining vital body functions, such as breathing and heart rate. So you’ll notice these are the autonomic processes. In other words, these are the processes that are going to happen whether you think about it or not. These are regulated by the medulla. And last but not least, we have the pons, which is involved in motor control and sensory analysis.

So once again, we have the midbrain, the medulla, and the pons. These 3 parts make up the brain stem. That’s it for this video, and I’ll see you in the next one.

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In this video, Leslie describes the cerebellum and explains how it’s involved in coordination of movements.

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Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, I’m going to be talking about the function of the cerebellum. Inside this video, first I’m going to answer the question, “Where is the cerebellum?”, then I’m going to answer the question, “What does the cerebellum do?” Lastly, I’m going to talk about what happens when there’s damage to the cerebellum. So let’s get right into it.

Where is the cerebellum? Well, the cerebellum is right here. In the last video, we spoke about the cerebrum, and this is the cerebrum here. In one of the future videos, we’re going to talk about this part here, that’s the brainstem. So when we’re talking about the cerebellum, we’re talking about this portion here, kind of at the bottom and to the back of the brain, tucked away right here. That is where the cerebellum is.

Now, let’s answer the question, “What does the cerebellum do?” First of all, the ‘cerebellum’ is Latin for ‘little brain’, so that’s where it comes from. It’s involved in coordination of movement, in other words, motor control. It receives sensory input from the body, and then it coordinates the motor output. It’s involved in posture, precision, and accurate timing.

To illustrate this, let’s imagine that you’re trying to climb a flight of stairs. So here are our stairs. You’re trying to get to the top, and let’s say that this is you over here. Ooh, great drawing. I think I should quit teaching and start drawing for a living. Okay, let’s make you happy, and let’s make you not bald. There we go. So this is you, and you’re trying to get to the top of the stairs. Now, what does that involve? That involves coordinating the motion of your legs, and your legs are going to go from the bottom step to the next step. Now, let’s start going to the next step here, but we’re going to pause here.

When I’m at this point, there are a number of things that your brain needs to know. Your brain needs to know that you’re at this point, and your brain needs to know that you are trying to reach this point. So what the cerebellum does is it takes the sensory input. You get stimulation from your eyes, saying “Okay, I can see what’s going on here. I can see where the next step is. I can see where I am at this point.” Based on that, it can coordinate the motion of your feet and your legs so that you can reach to that point.

So it brings in sensory input about where you currently are, where the position of your body is, and it looks at where you’re trying to reach. And if there are any adjustments that need to be made, it makes those adjustments.

If you’re at this point and, for example, the brain thinks that you’re at this point, the brain is going to try to get you to go down. What’s going to happen is you’re going to trip and fall. We don’t want that to happen, and fortunately, we have a cerebellum at the back of the brain that coordinates that taking input and motor output.

Let’s talk a little bit about what happens when there’s damage to the cerebellum. The cerebellum doesn’t cause motion, but it just coordinates it. So if there’s damage to the cerebellum, movement is still possible. However, it’s going to cause disorders in fine-motor control, posture, and motor learning.

For example, in the scenario that I just drew, if you’re trying to climb the stairs and the brain does not know exactly where your foot is, so it can’t really calculate how far you need to go, it can cause problems with you walking up the stairs. It can also cause jerky movements because the cerebellum is not able to fine-tune that motion and coordinate it in the way that it normally does.

That’s it for this video. In review, we’ve answered the question, “Where is the cerebellum?”, and then we answered the question, “What does the cerebellum do?” Lastly, we looked at what happens when there’s damage to the cerebellum. That’s it for this video, and I’ll see you in the next one.

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In this video, Leslie tells us about the cerebrum and the specific functions that each of its 4 lobes are responsible for.

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Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 25, I’m going to talk about the 4 lobes of the cerebrum and their functions. Inside this video, first I am going to answer the question, “What is the cerebrum?”, and then lastly, I’m going to talk about the 4 lobes and we’re going to look at what they do.

So first let us look at the question, “What is the cerebrum?” The cerebrum is the largest part of the human brain, and it’s involved in intellectual functions such as memory, attention, awareness, thought, language, and consciousness. These are the things that essentially make human beings human beings.

So let’s take a look at the 4 lobes of the cerebrum. We have the frontal lobe, the parietal lobe, the occipital lobe, and the temporal lobe. Let’s look at what they are involved in.

The frontal lobe is involved in processes such as reasoning, planning, speech, movement, emotions, and problem solving. So these are the types of things that are happening in the frontal lobe. Then we have the parietal lobe which is involved in movement, orientation, recognition, and perception. The occipital lobe is involved in visual processing, and this is why sometimes if you get hit at the back of the head, you see stars and so on. That has to do with visual processing. Then we have the temporal lobe which deals with auditory perception, memory, and speech.

So as you can see, there are a bunch of intellectual functions that are being controlled by the cerebrum of the brain. We have a general idea now of what regions are involved in what types of processing.

So in review, we answered the question, “What is the cerebrum?”, and then we looked at the 4 lobes and we spoke a little bit about their function. That’s it for this video. If you have any questions or comments, go ahead and leave them beneath this video. I’d be happy to answer your questions, and maybe even make a follow-up video to answer your specific question. You can always visit our website at Interactive-Biology.com if you want to get some more videos. That’s it for this video, and I’ll see you in the next one.