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=lDXVZOU_f_E

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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!

http://www.youtube.com/watch?v=L4F4zaRqQdk

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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.

http://www.youtube.com/watch?v=GpkD8AZTFCs

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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.

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In this video, Leslie clarifies how the myelin sheaths speed up the conduction of the action potential, in response to nicodube23′s question posted on YouTube.

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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. Inside this episode, Episode 24, I’m going to be talking about how myelin sheaths increase the speed of the action potential.

This is actually in response to a question that was asked by nicodube23 on YouTube. I’m not sure if I’m saying your name right, but if I’m not, please forgive me. This video is in answer to the question that you left. His question was placed on Episode 15 on YouTube where I spoke about saltatory conduction. This is what he says: “Why would the steps be bigger in myelinated versus unmyelinated axons? That’s the real question. What is the conceptual explanation for insulation increasing speed of conduction?” That is an excellent question, such a good question, that I felt the need to make this video to answer the question.

So this is what he’s referring to. Here we have a neuron, and the axon has these myelin sheaths, so I’m going to write here myelin sheath. Those are made by the Schwann cells. This is a Schwann cell that’s actually surrounding the axon and forming that myelin sheath. With saltatory conduction, I spoke about how the action potential jumps from one node of Ranvier to the next node. I called that saltatory conduction, and I said that is responsible for speeding up the signal. Since you’re taking bigger steps, it’s going to travel faster.

What I want to do is explain how that happens. When a stimulus comes along and causes the membrane potential to reach threshold, I said that voltage-gated sodium channels open. I’m going to say that this is a sodium channel. We know that we have a bunch of sodium ions on the outside, and when those channels open, sodium is going to rush in. When sodium rushes in, it doesn’t just stay here. Sodium has a positive charge, and that’s going to cause the positive charges that are close to it to be repelled, and sodium is actually also going to rush down the axon.

Now, this process of the charges moving along the axon, this is called electrotonic conduction. So what your have is a positive charge moving in, repelling all of the positive charges, and the positive charges are just travelling along the axon. One of the main benefits of this type of conduction is that it’s extremely fast. And that’s a good thing, you want it to be fast. However, we can’t really lie solely on electrotonic conduction. The reason for that is this also dies down, so the charge dissipates.

Let’s say the threshold is -55 millivolts. The membrane potential reaches the threshold, sodium rushes in, causing it to become very positive. That positive, I’ll put some pluses here, is going to repel the other positives and those charges are going to move along the axon extremely fast. Let’s say it goes down here. However, as it moves, that charge dies down. If we were to rely only on electrotonic conduction, if we have a long axon, the signal wouldn’t reach all the way to the end because it would die down until it gets beneath the threshold.

That’s a problem. So what we’re going to have here is, right here we have more voltage-gated sodium channels, we actually have them all along, but here they’re covered up. So even though there are sodium ions on the outside, they can’t get in because these voltage-gated sodium channels here are blocked.

As the charge moves down and it dies down, before it dies down too much, we have more voltage-gated sodium channels here, and those voltage-gated sodium channels are going to open and, of course, sodium ions are going to rush in. The charges can move again via electrotonic conduction. Before it does down too much, we can have more sodium ions rushing in here, and charge moving down by electrotonic conduction.

Now, the problem with this process is that it’s much slower. And if we were to rely on the voltage-gated channels opening to cause the action potential to go all the way down the axon, that would take much longer. And of course, if you put your hand on a hot stove, for example, you want that signal to travel extremely quickly. The good thing here is that it helps to increase the membrane potential, so I’m going to put an arrow going up, and Em stands for membrane potential. That causes a boost in the signal, so that this process can continue.

So we have an exchange of this fast process, with this slow process. But the way it’s paired makes it so that the signal can jump quickly from one node to the next node. So nicodube, to answer your question, the reason why it makes it faster is because electrotonic conduction is fast. Voltage-gated sodium channels opening is slower, so we’re pairing them up so we can have the perfect combination of a fast-moving charge and the boost to the membrane potential so that the fast-moving charge can continue until we reach all the way down the axon.

I hope that makes sense to nicodube and anybody else who has questions about saltatory conduction and how the myelin sheaths increase the speed of conduction. That’s it for this video, and I’ll see you in the next one.

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In this video, Leslie’s wife helps to demonstrate both the knee jerk and the eye blink reflexes.

Watch as Leslie explains how both of these reflexes work.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV. My name is Leslie Samuel. In this episode, Episode 23, we’re going to be talking about reflexes and how they work. We’re going to talk about the knee jerk reflex and we’re going to talk about the eye blink reflex. I have a very special guest here today. This is my wife, Marguerite.

Marguerite: Hello!

Alright, so this is my wife, and she’s going to help me to illustrate these 2 reflexes, and then we’re going to talk about how it happens.

Let’s first look at the knee jerk reflex. Sorry, I don’t have a tendon hammer here. I have a remote control, but the principle is still the same. What I’m going to do, here we have the patella bone, and right beneath that, we have the patellar tendon. What I’m going to do is try to hit her exactly on that patellar tendon, and we’re going to see what happens. So here we go. Ooh! One more time. Okay, so I hit, and what happens is, you know this already, but her leg kicks forward. There’s a muscle contraction happening, and we’re going to look at that process in a little while.

Now, what I want you to do is I want you to try not to kick. Can you do that?

Marguerite: Yup!

Okay, let’s do that. She’s trying not to kick, she’s tensing up or whatever she needs to do. We’re going to try it again. It still happened. You could still see that reflex. Even though she’s trying not to do it, once I stimulate it, something is going to happen and she’s going to do that reflex.

Now, we’re going to look at the eye blink reflex. What I’m going to do is I’m just going to take my hand and I’m going to do it towards her eyes. And you see that she blinked. I’m going to do it again, and you see that she blinked.

This is what I need you to do, honey. I need you to think about not blinking, and try hard not to blink. Can you do that?

Marguerite: I can try.

Okay, so she’s going to try. Alright, don’t blink. Try really hard. Okay, she didn’t blink. I’m going to try it again, and she didn’t blink. So she had more control of this reflex than she did with the knee jerk reflex. So now we’re going to talk about how this process actually works.

Let’s look at the mechanism behind the knee jerk reflex. Here, we have someone’s leg, and here’s the knee, and right here we have the patellar tendon. So let’s say I took a tendon hammer and I applied pressure to this tendon by just striking it there. What that’s going to do is it’s going to stimulate sensory neurons.

We spoke about the different types of neurons in Episode 2. We spoke about sensory neurons that send signals to the central nervous system, which is the brain and the spinal cord. We spoke about motor neurons that send signals away from the central nervous system and to muscles and organs and glands. And then we spoke about interneurons that are fully contained within the central nervous system.

Right here, what happens is when you strike the patellar tendon, that sends a signal via this sensory neuron. Let me show that in a different color. Via this sensory neuron to the spinal cord. So this is looking at the spinal cord as a cross-section. And what you’ll see is that makes a synaptic connection to a motor neuron, and that’s this other neuron that’s coming here. That neuron goes and stimulates the muscles to contract, causing the leg to be extended.

The key thing here is that when we look at this connection that’s happening inside the spinal cord, so if we look right here, we’ll see that it’s just a sensory neuron connected to a motor neuron. There are no interneurons whatsoever in this process. So I’m going to write here “no interneuron.” So because we don’t have any interneurons in this what we call a simple reflex arc, let me write that here, there’s hardly any processing happening here.

Once a signal comes in, a signal will go out, the muscles will contract, and the knee jerk reflex will happen, the leg will extend. The key here is that there is no interneuron, and because there’s no interneuron, there won’t be any significant processing happening. Once a signal comes in, a signal will go out.

Now, let’s look at the eye blink reflex. The eye blink reflex is a little different. I’m going to attempt to draw an eye here, looking at it from the side. I’m just going to simplify it. This is my eye, and here we have the pupil. This is a green-eyed person. So when I took my hand and I swung my hand towards my wife’s eye, she blinked.

What you have here is we have sensory neurons, once again, coming into the central nervous system, and I’m going to show this very simply. And then we have 1 interneuron, so I’m going to draw that interneuron here. And then, we have 1 motor neuron. This is my soma, and then we have the motor neuron sending signals to the muscles surrounding the eye. When this happens, it stimulates the muscles to contract, and then you blink your eye.

However, because there is 1 interneuron here, there is more control that you can have, because you can block the signal that goes to the motor neuron. So by putting that 1 interneuron here, we’re giving some more control. And you can control that eye blink reflex. It’s a little harder to control than other movements, but you can still control it.

Now, if you are to look at other movements that you make, like moving your hands and moving your legs and so on, there are many interneurons that are involved in that process. And the more interneurons you have, the more control you can have. If you look at something as complex as speech where you have muscles in the mouth and you have the vocal cords that you’re causing to vibrate, and there’s a lot of details that’s happening when you want to speak. In order for that to be the case, there needs to be many interneurons. The more interneurons you have in the process, the more control you’re going to have over the muscle contractions and over the movements.

So that’s how the reflexes work. That is why the knee jerk reflex happens whether you want it to happen or not, and that is why the eye blink reflex happens but you do have some control over it. These are tests that doctors use to see if the nervous system is functioning correctly, and it gives them specific details about specific aspects of the nervous system functioning.

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This is a video answering Akbar’s question regarding the difference between the inactive and closed states of voltage-gated sodium channels.

Watch as Leslie explains this difference using a box.

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 today’s episode, I’m going to be answering a question that was left on my blog. On Episode 12 where I spoke about the absolute and relative refractory periods, a question was left by Akbar, and his question was, “Can you please elaborate a bit more on the inactive state of the sodium channel? How does it differ from the closed state?” That’s a very good question and I’m glad he asked it.

In order to illustrate the difference, I’m going to use this box here. The type of box doesn’t matter too much. Let’s say that this box is a voltage-gated sodium channel. There are 3 states that this box can be in. It can be closed, which you can see right now, and it can be open, and it can be inactivated. The way this works is we have 2 gates. These are the 2 gates. I’m going to call this the activation gate, and I’m going to call this the inactivation gate.

So we have a stimulus that comes along, and the stimulus causes the membrane potential to become more positive, and it reaches the threshold. Now, the cool thing about this activation gate is that it’s positively charged. Imagine that you have a bunch of positive charges inside here, and let’s say it’s inside the cell, what is that going to do to the positive charge of the gate? Now, you probably know that like charges repel, and opposite charges attract. Well, we have like charges here, and as that charge builds up, that positive charge is going to cause the positively charged activation gates to open.

When that happens, within 0.5-1.0 millisecond, the inactivation gate automatically closes. That has to do with the structure of the gate, the structure of the channel, and a few different properties that I’m not going to go into. But basically, the idea is once it opens, this just closes automatically after a certain period of time. That period of time would be 0.5-1.0 millisecond. Once it’s inactive, you can’t re-stimulate it. The only way for you to re-stimulate the channel is that it needs to be reset to the closed state. As we said, the activation gate is positively charged, so when the second phase of the action potential happens and potassium rushes out of the cell, the cell becomes more negative, and as it becomes more negative, this gate now gets pulled in so that the channel closes.

So the difference between inactive and closed is: inactive means that the inactivation gate is closed; when it’s fully closed, it’s when both gates are closed, so the activation gate now is closed, and it’s ready to start another action potential.

I hope that clarifies it for you, Akbar, or anyone else that’s listening. If you have any more questions about any of the topics, please feel free to leave them in the comments below, and like I said, like you’re seeing here, I’d be more than happy to make a follow-up video or answer your question in the comments. That’s it for this episode, and I’ll see you in the next one.

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So what’s the deal with drugs? Why do people get addicted? In this video, Leslie talks about how addiction works at the level of the Neurotransmitter.

Wanna know how it works? Curious? Watch the video

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 21, I’m going to talk a little bit about the mechanism of addiction. Inside this video, I’m first going to answer the question “What is addiction?”, then I’m going to talk about the mechanism of addiction, and lastly, I’m going to look at some specific drugs and how they affect neurotransmitters. So let’s get right into it.

There are 2 definitions of addiction that I want to look at:

1. Addiction is believing that you need a drug to feel good or function normally.
2. Addiction is developing a chemical need for a drug.

The second one is the one that I’m going to be talking about. How do you develop a chemical need for a drug which leads to you becoming addicted to that particular drug?

Let’s look at the mechanism for addiction. What usually happens is, when you take a drug, it multiplies the effect of a specific neurotransmitter. Now, we’ve been talking about neurotransmitters, and we saw how that can lead to a signal in post-synaptic cells. You can always go back to previous episodes to look at how that works. What a drug does is it makes the effect of a specific neurotransmitter much stronger, and that can have some significant effects.

One of the effects is that the nervous system starts to slow down the production of the neurotransmitter. What usually happens is there’s an artificial increase in the effect of that neurotransmitter, so the brain is saying, “Wow, there’s too much of that neurotransmitter there.” So the nervous system actually slows down what it would normally produce. This is a neurotransmitter that the body needs, and since the nervous system slows down the production, you become dependent on that substance that you’re taking in order to return back to normal. So the brain is saying, “Whoa, there’s too much of that neurotransmitter out there. Let me stop what I’m doing.” And in order for you to feel normal again, you need to take more of that substance, more of that drug.

So that’s the general mechanism for addiction. Of course, every drug is going to have a different effect, and of course, there are other effects that these drugs have, but right now, we’re just talking about the specific process of addiction.

So let’s look at some specific drugs and the neurotransmitters they affect. Caffeine is one of the most popular drugs. Caffeine affects the neurotransmitter dopamine. Dopamine is known as the feel-good molecule of the nervous system. There’s a reward circuit that responds to pleasurable experiences by releasing this neurotransmitter.

Another drug that has an effect on that same neurotransmitter is cocaine. That also affects dopamine. This results in a really strong dopamine effect, and the brain shuts down the production of dopamine. In order for you to feel good again, you need to take that drug. Of course, cocaine is on a totally different level than caffeine, and of course, it’s going to have many other effects that we’re not going to go into in this video. So when you take these drugs, it’s artificially increasing a neurotransmitter that normally makes you feel good, and you get an intense feeling of pleasure that’s more than normal, and that also can contribute to the addictive effect of these drugs.

Another common drug is nicotine, and that affects the neurotransmitter acetylcholine. We’ve looked at that neurotransmitter, we’ve seen that it’s an excitatory neurotransmitter that causes EPSPs, excitatory post-synaptic potentials. Nicotine has an effect on this neurotransmitter.

Another drug is LSD, and that has an effect on the neurotransmitter serotonin.

So you can see these different drugs are going to have different effects on different neurotransmitters and how the body responds to these neurotransmitters. When the nervous system stops producing or slows down the production of that neurotransmitter, you need to take more of that drug in order to feel normal.

That’s really it for this video. That’s the general overview of how the process of addiction works. If you have any questions, as usual, go ahead and leave your questions below in the comments section. I’ll be happy to answer your questions, and maybe even make a video to answer your specific question. 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 facilitation and illustrates how it causes a stronger and longer signal in the post-synaptic 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, I’m talking about the process of facilitation, and we’re going to look at how this leads to a longer and stronger response in the post-synaptic cell.

Here, I’m looking at a neuron, and let’s say there’s an action potential that comes along this axon and enters into the axon terminal. I’ve drawn this terminal a little bigger than the previous ones because there’s a lot of stuff that I wanted you to see in here. As we’ve mentioned before, when the action potential reaches the axon terminal, it causes voltage-gated calcium channels to open, calcium ions rush in and that causes the vesicles to fuse with the membrane, releasing neurotransmitters, causing a signal in the post-synaptic cell. Now, this calcium that rushes in also causes depolarization because this has a positive charge. Usually, what happens after that is voltage-gated potassium channels open and potassium rushes out of the cell, repolarizing the membrane, ending the signal, ending calcium coming in, ending the neurotransmitter release.

In the process of facilitation, we have this facilitatory neuron, or you can call this a pre-synaptic synapse, and this neuron releases the neurotransmitter serotonin. When it releases that neurotransmitter serotonin, that binds to the receptor, and this is a metabotropic receptor, and this one specifically activates a G protein. That G protein activates adenylate cyclase. Adenylate cyclase converts ATP to cyclic AMP, which then activates a protein kinase, specifically protein kinase C, so I’ll put a C right here. That protein kinase phosphorylates the voltage-gated potassium channels, and what that does is it shuts those channels so potassium cannot leave as easily as it would have in a regular situation.

So the net result here is, we have an action potential that comes down, we have depolarization, but instead of repolarization happening quickly, repolarization takes longer to happen. It causes the action potential, the signal here, to last longer. And, of course, what that’s going to do is it’s going to cause more vesicles to fuse with the membrane, and you’re going to end up with more neurotransmitters being released. That, of course, is going to result in a greater signal in the post-synaptic cell.

So once again, action potential comes along, voltage-gated calcium channels open, calcium ions rush in. But we have this secondary neuron, a secondary synapse that releases serotonin, binds to the receptor, activates a G protein, which activates adenylate cyclase, converts ATP to cyclic AMP. That activates a protein kinase C, which phosphorylates the voltage-gated potassium channels, causing them to close, allowing the signal to last longer and for more neurotransmitters to be released, resulting in a stronger signal, a longer signal in the post-synaptic cell.

That’s really it for this video. If you have any questions, go ahead and leave them in the comments, and I’ll be happy to answer them. That’s it for this video, and I’ll see you in the next one.

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When post-synaptic potentials reach the neuron, they can be added up through the process of summation.

Watch as Leslie explains this process and expounds on the 2 types of summation.

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 19, I’m going to be answering the question “What is summation?” and I’m going to talk about the 2 types of summation. So let’s get right into it.

Summation is basically the addition of post-synaptic potentials. To illustrate this, I’m going to draw our membrane potential graph, with membrane potential on the Y-axis, Em, and time on the X-axis. I’m going to start with our resting membrane potential somewhere around -70 millivolts, so let’s say this is -70. Now, we’ve spoken about threshold, and we said that in order for there to be an action potential, the membrane potential needs to reach that threshold, and I’m going to say that’s around -55 millivolts.

So an action potential comes down an axon, it reaches the axon terminals, neurotransmitters are released, and that causes an excitatory post-synaptic potential in the post-synaptic cell. What you’re going to see there is there’s going to be a little bump in the membrane potential. We know that the threshold is up here, so that bump is not going to be enough to cause an action potential.

So what needs to happen is we get an excitatory post-synaptic action potential, and before the first one finishes, another one comes along, raising the membrane potential even more, and that process continues over and over until eventually, we have enough stimulation to cause the membrane potential to reach threshold. And then, we get the action potential with our depolarization, our repolarization, our hyperpolarization, and then the action potential is finished.

So that’s what we’re talking about with summation. We’re basically adding these post-synaptic potentials. Remember, sometimes we can get excitatory post-synaptic potentials, we can get inhibitory post-synaptic potentials that bring our membrane potential even further away from the threshold. But we’re basically adding them so that we can reach that -55 millivolt threshold and cause an action potential.

With that understanding, let’s look at the 2 types of summation:
1. Temporal summation
2. Spatial summation
I’m going to do a drawing to illustrate both. With temporal summation, what we have is a pre-synaptic neuron, so let’s just draw an axon, and I’m going to simplify it by making just 1 axon terminal, and that makes a synapse with a post-synaptic neuron, so here’s my neuron. Here we have the soma, and here we have the axon. What happens is a signal comes along this axon, comes to the axon terminal, releases neurotransmitters, and that causes an excitatory post-synaptic potential in this cell. That is where we see the first bump. Now, if it sends that signal and it sends another one quickly and it continues doing that, that’s going to cause the membrane potential to go up and up until it reaches the threshold and causes the action potential. This is temporal summation.

Now, that’s different from spatial summation. With spatial summation, we have an axon here, and I’m just going to draw 1 axon with 1 terminal, of course that’s simplified, that connects to another neuron. However, we also have another axon that comes and we have an axon terminal that connects to the same neuron.

What’s going to happen here is this one can cause a signal, an excitatory post-synaptic potential, and before that dies off, we can have another signal coming from this other cell. So we have 2 separate neurons causing responses in this cell, and of course, we get the same result where the membrane potential goes up, and when the next one fires, it goes up again, and this one can fire again, that causes it to go up, and then it eventually reaches the threshold, causing our action potential. That is spatial summation.

So an easy way for you to remember this, at least this is what works for me, spatial summation is separated by space, because we have 2 separate neurons that are firing. Temporal summation is the same neuron firing, but each signal is separated by time. So temporal summation is separated by time, same neuron. Spatial summation is separated by space, because there are 2 separate neurons.

That’s all the content for this video. We’ve looked at the 2 types of summation and we’ve answered the question “What is summation?” If you have any questions, go ahead and leave a comment below, and I’d be happy to get to it. That’s it for this video, and I’ll see you in the next one.

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In this video, watch as Leslie explains how agonists and antagonists affect the receptor sites of the 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 18, I’m going to be talking about agonists and antagonists. It almost sounds like a plot for a movie, but it’s not a movie, unless it’s a movie happening inside your body. Anyhow, for today, let’s get into what we’re going to be talking about.

The first thing we’re going to talk about is “What is an agonist?” An agonist is a molecule that mimics the effect of a neurotransmitter, so it does what that neurotransmitter would normally do. An example of that would be succinylcholine mimics the neurotransmitter acetylcholine. So what I’m going to do is I’m going to draw the receptor here, and here we have the cell membrane of the neuron. I’m going to draw it a little different than I’ve been drawing it before. I’m going to have these as the receptor sites. This is where the acetylcholine normally binds to the nicotinic receptor.

I’m going to draw acetylcholine here, but I’m not going to draw it coming here. What I’m going to do is I’m going to draw something that’s slightly different, let’s just say it’s a different color. It’s a similar shape to acetylcholine, and we’re going to call this succinylcholine. When that comes here and it binds to the receptor, same thing here, it comes and it binds to the receptor, the channel opens, which is what it would normally do if acetylcholine binds. And then, sodium ions on the outside end up coming inside the cell. So this would be an example of an agonist. It’s not acetylcholine, it’s something else, and let’s say, in this case, it’s succinylcholine, and that comes, binds to the receptor and causes a similar response. That is an agonist.

Now, let’s look at what an antagonist is. You can probably guess just by reading the word, but an antagonist is a molecule that opposes the effect of a neurotransmitter. So it does the exact opposite. An example of that would be curare, which is an antagonist to acetylcholine that can actually block the binding sites for acetylcholine. So here, we have our nicotinic receptor again, and it’s in the membrane of the cell, and here we have the binding sites.

Out here, we have acetylcholine that wants to bind. However, we have something else that’s around that’s not exactly like acetylcholine and let’s say that its shape looks something like this. That binds to the receptor, and what that does is it blocks the receptor site. So acetylcholine wants to bind and it wants to cause that channel to open, but it’s being blocked so that it cannot bind, and it cannot open the channel for sodium to come in. This would be an example of what curare does. It’s an antagonist, and in fact, curare can cause muscles to become paralyzed because they cannot be activated and sodium cannot rush into the cell, exciting the cell, and exciting the muscle to contract. So that can be a serious thing if you have curare binding to these receptor sites.

That’s really all for this video. I hope you understand the difference between an agonist and an antagonist. If you have any questions or comments about that, go ahead and leave them below. I’ll be happy to answer your question, and maybe even make a follow-up video answering your specific question. That’s it for this video, and I’ll see you on the next one.

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After neurotransmitters are released from the cell, they bind to receptors on the next cell.

In this video, Leslie explains how the two different types of receptors – the ionotropic and metabotropic receptors – work to bring about various responses in the cell.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 17, I’m going to be talking about 2 types of receptors. We’ve been talking about the nervous system, we’ve been looking at neurons, and we’ve seen how the action potential starts at the axon hillock, the signal travels all the way down the axon, down to the axon terminals. In Episode 16, we looked at how the neurotransmitters are released from the axon terminals, and they bind to receptors on the next cell.

What we’re going to be doing is looking at those receptors because there are 2 basic types of receptors:
1. Ionotropic
2. Metabotropic

What we’re going to do is we’re going to look at the ionotropic receptors first. With ionotropic, these are very fast-acting receptors. What I’m going to do is I’m going to attempt to draw one now. Let’s say here we have a receptor, and this is a cell membrane. We have the signal that comes along the axon of the preceding cell, and it releases neurotransmitters. I’m going to say these little dots here are neurotransmitters, and they’re in the synaptic cleft.

What’s going to happen if it’s an ionotropic receptor, the neurotransmitter is going to come and it’s going to bind to the receptor. The way these receptors are set up is relatively simple. When the neurotransmitter binds to the receptor, that causes the channel to open. So, I’m going to draw this showing that now there’s an open space. And then, if there are ions that are outside the cell that are specific to that channel, those ions can then enter the cell. So it’s very fast-acting. The neurotransmitter binds to the receptor, and then the channel opens so that the ions can travel inside the cell. Once again, these are ionotropic receptors.

Now, of course, there are going to be different types of neurotransmitters and different types of receptors that are going to act in this way. I’m going to take the example of acetylcholine as a neurotransmitter. So we’re going to start with ACh, and that’s for acetylcholine. We’re going to call these neurotransmitters acetylcholine, and the receptor that’s the ionotropic receptor for acetylcholine is called the nicotinic receptor. The reason it’s called nicotinic is because this is the receptor that nicotine acts on, and we’re going to talk about that in a later episode.

So, acetylcholine comes, and actually 2 acetylcholines bind to the nicotinic receptor, and then that causes sodium ions to rush in. And now you know that sodium ions are going to have a positive charge, so what do you think that’s going to do to the membrane of the cell? Well, of course, that’s going to make it more positive. So I’m going to look at it here. Let’s say I’m looking at voltage or membrane potential on the Y-axis, and I’m going to have time on the X-axis. This is the resting membrane potential.

When something like this happens that causes sodium to come in, that can cause the membrane potential to get this little bump here. So it increases a little from that sodium rushing into the cell. Because this is becoming more positive, we’re going to call this an excitatory (it’s getting it excited) post-synaptic potential. EPSP, excitatory post-synaptic potential. Because it’s acetylcholine binding to the nicotinic receptor, that’s going to cause sodium ions to rush in, causing an excitatory post-synaptic potential.

Now, there’s another type of neurotransmitter, 2 examples would be GABA and glycine (forgive my writing there, but I think you get it.) When these bind, let’s say this is GABA or glycine, what that is going to do is it’s not going to cause not sodium ions, but chloride ions, and let’s say this is chloride, Cl-, to rush into the cell.

If a negative ion rushes into the cell, what is that going to do? Well, you probably guessed it. Instead of causing an excitatory post-synaptic potential, that’s going to cause an inhibitory post-synaptic potential, or an IPSP. So if it’s a positive ion rushing in, you get an EPSP. If it’s a negative ion rushing in, you’re going to get an IPSP. This is a really fast-acting process: neurotransmitter binds, channel opens, ion rushes in.

Let’s go to the next type of receptor, and that’s called the metabotropic receptor. This is going to be a little more complicated, because what we have here, just like before, we have a receptor in the membrane. And just like before, we have neurotransmitters that are outside the cell. But what’s different here, is that inside the cell, associated with this receptor, we have a G protein.

What happens is this neurotransmitter comes and it binds to the cell, just like before, and instead of opening a channel, what that does is it activates the G protein. And then this G protein then goes on to activate a second messenger system where there can be multiple processes that are happening, causing a certain response on the inside of the cell.

So this is a slower process in that there are multiple processes happening, and it causes a different type of response. That response can be a number of different things, and we’re going to talk about that a little later.

An example of a metabotropic receptor would be the muscarinic receptor. With the muscarinic receptor, acetylcholine is still the neurotransmitter, so ACh, and that binds to the receptor that activates a G protein. When it activates a G protein, a number of processes happen that cause multiple responses, depending on the type of muscarinic receptor we’re dealing with. One of the features that we have here is for every neurotransmitter that binds, that can activate a G protein, and whatever process this is can happen multiple times, and then this process this is can happen multiple times, so that we get a greater response on the inside.

For example, I’m just going to take a random number. Let’s say here we activate 1 G protein, and this process can happen 10 times, and each one of those can cause this next process to happen 10 times. So this second messenger system can result in a significant amount of amplification, so that we can get a significantly greater response.

Those are the 2 types of receptors: we have the nicotinic receptor and we have the muscarinic receptor. If you have any questions about this, you can leave them in the comment section below, or you can just leave a comment letting me know what you think about the format of what I’m doing, and even give suggestions for future episodes. That’s it for this video, and I’ll see you on the next one.

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When the action potential reaches the axon terminals, something needs to happen in order to transfer that signal from one neuron to another.

Watch as Leslie explains the role of neurotransmitters and how their release results in a signal in other cells, organs, or glands.

Enjoy!

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 16, I’m going to be talking about the neurotransmitter. We’ve been talking about the nervous system, we’ve been talking about neurons, and we’ve been talking about the action potential and how that travels along the neurons all the way to the ends of the neurons. What we’re going to do today is we’re going to focus a little more closely at the end of the neurons, the place that we call the axon terminal.

Now, neurons do not exist in isolation. They are interconnected, they connect to other neurons, as you can see right here. There’s a connection here, you can see there’s another connection here. Basically, when there’s a signal in one neuron, that can send a signal to many other neurons or glands or organs. This is the way the nervous system communicates, and there needs to be these connections, and signals need to go from one neuron to the next.

What I’m going to do is I’m going to zoom in on this connection here and we’re going to take a closer look at it. So we’re looking at that connection, and there are a few terms that you need to understand. The connection between the neurons, we call that the synapse. The synapse is the connection between one neuron and another neuron, or between one neuron and another cell, organ, or gland. We are basically talking about the place where neurons connect with other cells.

Another term that you need to know is the synaptic cleft, and the synaptic cleft is basically this space here that’s between the neurons. Most neurons don’t connect physically. There’s a small space between those neurons where they connect and there are some important things that are happening there, and we’re going to look at those things today.

Another term that you need to know would be the synaptic vesicles, and you can see there are a number of vesicles in here. What’s unique about these vesicles is that inside of those vesicles, we have neurotransmitters. You can see examples of neurotransmitters here. This is a neurotransmitter, and we have 3 in here, 2 in here, 1 in here. These are all neurotransmitters.

Another term that we need to be familiar with would be the receptor. The receptor is the protein or the part on the receiving cell that binds to the neurotransmitter. You can see a perfect example of one here.

Some other terminology that’s not on this image is, since we’re calling this the synapse, we have 2 membranes. We have this membrane here, and we have this membrane here. The membrane that comes right before the space, we call the pre-synaptic membrane. So that’s this membrane here. And the membrane that comes after the space, and that would be this membrane here, you guessed it! We call that the post-synaptic membrane. So those are the terms that I want you to be aware of as we go into talking about what happens when the action potential reaches the axon terminal.

We’ve spoken about the action potential, and the action potential travels along the axon. I want you to imagine with me an action potential coming down this axon and reaching the axon terminal. Now, there are a number of things that happen when the action potential reaches the axon terminal. One of the most important things that’s happening is we have voltage-gated calcium channels that open. When voltage-gated calcium channels open, calcium ions that are concentrated outside (I’m going to write Ca++) are going to rush into the cell.

This is a very important event because it causes something that’s very significant. It causes these synaptic vesicles to fuse with the pre-synaptic membrane, and you can see an example of that happening right here. When the synaptic vesicle fuses with the pre-synaptic membrane, that causes the neurotransmitter to be released into the synaptic cleft. You can see an example of a neurotransmitter that’s released right here, and of course, there’s another one right here.

Now, what then happens is also very important. The neurotransmitter binds to the receptor. When the neurotransmitter binds to the receptor, that can cause a signal in the receiving cell. So we can have a signal in this cell because neurotransmitters are being released and that binds to the receptors, and that causes a signal in the receiving cell.

This is how we can go from one neuron to the next neuron. Signals are travelling rapidly and they need to be routed to the right place. The way the neurons are going to communicate with each other is by this process of releasing neurotransmitters. That’s all the content for this video. If you have any questions about it or any comments, go ahead and leave a comment beneath this video in the comment field. I’d be happy to answer your question, or even make a follow-up video to answer your specific question. That’s all for this video, and I’ll see you in the next one.

http://www.youtube.com/watch?v=M3u7v0RXkok

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The action potential travels rapidly down the axon. Why? Because of the process of saltatory conduction.

In this video, I talk about how that process works.

Question? Comments? Leave them below

- Leslie Samuel

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, I’m going to be talking about saltatory conduction. We’re going to look at how this process is responsible for having the action potential move quickly down the axon.

We’ve been talking about the action potential, and we’ve shown that in order for an action potential to happen, voltage-gated sodium channels need to open. And once those voltage-gated sodium channels open, sodium ions rush in, causing the membrane potential to become more positive and initiating the action potential.

Now, there’s something that you need to understand here. The process of voltage-gated sodium channels opening is significantly slower than sodium rushing along the axon once it’s in the axon. So sodium moving along the axon happens much quicker than the voltage-gated sodium channels opening.

You can think about it like this: if you’re in your car, and you’re trying to get into your garage, you can do that really quickly. However, in order to get into the garage, you have to wait for the garage door to open. And it’s a similar concept: voltage-gated sodium channels need to open, and that’s a little slower than the movement of the ions along the axon. Keep that in mind as we look at the example that I’m going to give right now.

To illustrate this, I am going to step back all the way back here. What I’m going to do is I’m going to take 4 steps forward. And I’m going to just go 1, 2, 3, 4. Now, those were 4 very small steps, and I’m going to take 4 steps backwards now again. 1, 2, 3, 4, and I’m in the starting position. Now, what I’m going to do is I’m going to repeat the same process but I’m going to take bigger steps. 1, 2, 3, 4, and you can see I’m much closer to the camera. I’m going to do the same thing and go back now. 1, 2, 3, 4.

Now, which one of these is faster motion? Of course, you’re going to say the second time, when I took the bigger steps, I was moving significantly faster. If we look at the axon, and let’s just look at a picture of an axon right now. What you will see is that we have Schwann cells that cause myelin sheaths to wrap around the axon. What you will notice by looking at this is you will see that there are little spaces between the myelin sheaths. These spaces are called the nodes of Ranvier. At these nodes, this is where we have voltage-gated sodium channels and voltage-gated potassium channels, but here is where the channels can open and allow ions to come in.

Because these channels are concentrated in these nodes of Ranvier, these are the places along the axons where the channels are going to open to allow sodium to come in. Once sodium comes in, it can jump from that node to the next node very rapidly. And then when sodium comes in at this point, it can go from that node to the next node very rapidly.

In other words, it’s as if the signal is jumping from one node to the next node to the next node, and that causes it to go faster, because it doesn’t have to wait for voltage-gated sodium channels to open all along the axon. It’s just like I was showing before. When I took bigger steps, I moved significantly faster.

Saltatory conduction is like taking these bigger steps, jumping from one node to the next node to the next node, and that helps the action potential to travel significantly faster. I hope that makes sense. As usual, if you have any questions, you can go ahead and leave your questions or your comments in the comments section below, and I’d be happy to answer your questions. That’s it for this video, and I’ll see you in the next one.

http://www.youtube.com/watch?v=yRRW0DNt95w

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Why does the action potential travel in one direction down the axon? Why doesn’t it go in reverse? Are there features about the axon that makes that happen?

Watch the video and find out.

Enjoy!

- Leslie Samuel

Transcript of Today’s Episode

Hello and welcome to Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. In this episode, Episode 14, we’re going to be looking at the journey down the axon. In other words, we’re going to look at how the action potential actually travels down the axon so that it reaches the axon terminals.

To illustrate this, I’m going to attempt to draw a neuron, and I’m going to start with the soma, which is the cell body. Then I’m going to draw the axon. I’m not going to draw the axon terminals, but I’ll just write here “AT” for axon terminals. Over here, we have the soma, and of course, this will be the axon. Now right here where the soma meets the axon, as we’ve seen in earlier videos, this is called the axon hillock, and this is the first place we see voltage-gated channels.

So, when a stimulus comes and causes the membrane potential to reach threshold, what we said happens is voltage-gates sodium channels open, and sodium rushes in. I’m going to write here “Na+”, so that’s sodium ions, and I’m going to just put a few of those outside the axon. So there we have it, sodium ions concentrated outside the axon.

A stimulus comes along, voltage-gated sodium channels open, and then sodium, because of its driving force, rushes into the cell. When it rushes into the cell, it just doesn’t go into the cell and stay in one place. Of course, it’s going to travel along the axon and it’s free to travel in both directions. When that comes in and it moves down the axon, that’s going to make the membrane potential more positive since sodium has a positive charge.

As it goes down here, it’s going to open more channels, and more sodium ions are going to rush in, and of course those are free to travel in either direction. The same process will continue: membrane potential goes up, sodium rushes in, travels in either direction. That’s going to continue over and over until it reaches the terminals.

Now, one of the questions you might be asking at this point is, “If the sodium ions can travel in either direction, why is it that we have an action potential that just travels in one direction?” That’s a very important concept for you to understand. We spoke about the refractory period. When the channels over here open and the sodium ions travel down, that causes these channels to open and sodium comes in and goes in either direction.

However, the voltage-gated sodium channels that are on this side are in their refractory period. If you remember what we said in the episode about refractory periods, when it’s in the absolute refractory period, you cannot stimulate the voltage-gated channels to open again. You have to wait for it to be reset to closed before you can re-stimulate it.

So all those sodium is rushing in and travelling in both directions, the signal is only going to travel down the axon because of the fact that the previous voltage-gated sodium channels, the ones that are closer to the soma in that direction, those are going to be either open or inactive. And it needs to wait for them to be reset to closed before they can be re-stimulated to fire. This is why the action potential will only travel in one direction.

That’s the entire concept for this video. As usual, if you have any questions, feel free to leave it in the comments below, and I’ll be happy to answer your question, and maybe even make a video to answer your specific question. That’s it for this episode, and I’ll see you in the next one.

http://www.youtube.com/watch?v=HnKMB11ih2o

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So we’ve gone over Depolarization, Repolarization and Hyperpolarization in some detail. It’s time to do an overall review.

Watch the video above to put everything into perspective and solidify your understanding.

And as usual, you may leave your questions/comments below.

- Leslie Samuel

Transcript of Today’s Episode

Hello and welcome to Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel. This is Episode 13, where we’re going to be talking about the action potential. I’m basically going to be giving you a review of the concepts that we’ve been talking about up to this point when it comes to the action potential.

Over here, we have our neuron. The part of the neuron that we’re going to be focusing on is the axon, so that’s this region here, starts here and it goes to about there. Now what I’m going to do is I’m going to take a section of the neuron, let’s say I’m going to take this part here and I’m going to draw it down here. So here we have the axon. This is inside the axon, and this is outside the axon.

If you remember from a previous episode, outside the axon, we have a lot of sodium ions. So I’m going to draw sodium ions here, and they are all outside the cell. Now let’s look over here. Here we have a stimulus that’s happening. You can see there’s a first stimulus that does not reach threshold, so nothing happens. Another stimulus comes, it does not reach threshold, so we still do not get an action potential. If we have a stimulus that’s strong enough, and I’m going to draw another stimulus in here. So let’s say we have a stimulus that’s that big. That’s going to reach the threshold and cause an action potential.

When that happens, voltage-gated sodium channels are going to open, and that’s going to cause sodium to rush into the cell. Of course, that’s going to start at the axon hillock. Sodium is going to rush in, making the membrane potential even more positive, causing more channels to open, more sodium to rush in along the axon.

What is that going to do to the membrane potential? You can see right here, this is where we get depolarization. The membrane potential goes up, and it’s trying to reach the Donnan equilibrium for sodium ions. That equilibrium potential is somewhere around 58 millivolts. Sodium is rushing in because of the driving force causing sodium to go in. Sodium wants the membrane potential to go up to its Donnan equilibrium, and that is around 58 millivolts. At this point, voltage-gated potassium channels have enough voltage in order for them to open.

So I’m going to erase all of this now, and we’re going to take at the axon again, I’m going to draw it here in blue. Inside the cell, we have a bunch of potassium ions. Now we have such a positive charge on the inside that potassium ions want to leave, because positive repels positive. When voltage-gated potassium channels open, potassium can now leave the cell. So we have a lot of positive leaving the cell, and what that is going to do is cause repolarization, where the membrane potential is going down. Just like with sodium, potassium wants to reach its equilibrium potential, which is somewhere around -93 millivolts. That is why the membrane potential is going down as it’s leaving, because potassium wants the membrane potential to be at -93 millivolts. That is where it is most comfortable.

Considering that the resting membrane potential is around -70, the membrane potential goes significantly lower than that -70, and this phase we call hyperpolarization. All along this process, we have sodium-potassium pumps that are pumping 3 sodium ions out of the cell, and 2 potassium ions back in. That’s going to cause the membrane potential to eventually reach back to its resting state.

This is the entire action potential, looking at depolarization, repolarization, hyperpolarization, and it getting back to the resting state. I hope that makes sense. If you have any questions, feel free to leave them in the comments below. I’d be happy to answer your question, and even maybe make a video answering your specific question. That’s it for this video, and I’ll see you in the next one.

http://www.youtube.com/watch?v=Gsf9IB-wQdU

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Refractory Period? What is that? If you are asking that question, then you want to watch this video.

It explains why you can’t stimulate another action potential at certain times regardless of how strong the stimulus is and why it takes a stronger stimulus to cause another action potential in specific situations.

Check it out, and if you’re left with a question or comment, leave it below.

- Leslie Samuel

Transcript of Today’s Episode

Welcome to another episode of Interactive Biology TV. My name is Leslie Samuel. In this episode, Episode 12, we’re going to be talking about the absolute and relative refractory periods. But before we talk about these refractory periods, let’s look a little bit at voltage-gated sodium channels. Now, we’ve been looking at the action potential, and we’ve said that when a stimulus comes and it makes the membrane potential go above the threshold, we get an action potential. The reason why we get this action potential is because voltage-gated sodium channels open.

Now, voltage-gated sodium channels are very unique, in that they have 3 states that you can find them in. They can either be closed, or they can be open, or they can be inactive. How this works is very simple. They have an activation gate, and they also have an inactivation gate. When the stimulus causes them to open, the activation gate opens, and after 0.5 to 1 millisecond, the inactivation gate automatically closes. What is special about these voltage-gated sodium channels is that once it’s open or inactive, it cannot be re-stimulated to open, because it’s either already opened, or it’s inactivated. With that in mind, let’s go and take a look at what causes the absolute and relative refractory periods.

Here, I am looking at a neuron, and you can see the neuron over here to the right. You know by now the parts of the neuron. Here we have a soma, and then here we have the axon. The main part that we’re going to look at today is what is happening in the axon, like we’ve been looking at in the last few episodes.

If I’m going to look at an action potential and I’m looking at what is happening to the membrane potential, here you can see that we have a stimulus, but it doesn’t cause an impulse. We have another stimulus, but still it does not cause an action potential. But if the stimulus reaches the threshold, we have depolarization. For a review of depolarization, see the episode on depolarization.

What this means is voltage-gated sodium channels (I’m going to write Na+ for sodium ions) open, and sodium rushes into the cell, causing the membrane potential to become more positive. Now, while that is happening, this means that the voltage-gate sodium channels are either open, or they are inactive. So they open first, and after a short period of time, they become inactive. While this is happening, no matter what you do, you cannot cause another action potential, because this one is already on the way, and the voltage-gated sodium channels are either open or inactive. So it does not matter what you do, we will not get another action potential. This is called the absolute refractory period. So we have the ARP, for the absolute refractory period, because the voltage-gated sodium channels are either open or inactive.

As I said in the previous slide, in order for another action potential to happen, those voltage-gated sodium channels need to be reset to close. When we reach the repolarization phase and potassium rushes out, the membrane potential starts going down. As it starts going down, the voltage-gated sodium channels start resetting to their closed state. Once they start resetting to their closed state, you can stimulate it to do another action potential.

However, if there are only a few sodium channels reset, it’s going to take a significantly stronger stimulus to cause the membrane potential to reach the point where we can stimulate the action potential to happen again. I’m going to say that again. When the voltage-gated potassium channels open and potassium ions rush out of the cell, the membrane potential is going to start going down because it’s repolarizing. Once that starts happening, voltage-gated sodium channels start being reset to their closed state. You can stimulate it to have another action potential, but it’s going to take a stronger stimulus since you have fewer channels being reset. That is the relative refractory period (RRP). And that continues, more and more channels are being reset to the closed state, and when they’re all reset to the closed state, that is the end of the relative refractory period.

So you stimulate the axon, you get an action potential, voltage-gated sodium channels are either open or inactive, and you cannot stimulate it again. That is the absolute refractory period. Once they start resetting, you have the relative refractory period, where you can stimulate another action potential, but you will need a stronger stimulus. So that’s the absolute and the relative refractory periods.

I hope it makes sense. That’s all for this video, and I’ll see you in the next one.

http://www.youtube.com/watch?v=JbCIvMz0yvc

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First there’s Depolarization, then Repolarization and finally – Hyperpolarization. Want to know what it’s all about? Watch the video.

It’s only 2 minutes and 33 seconds, but it packs a punch.

Any Questions or Comments? Leave them in the comments section below.

- Leslie Samuel

Transcript of Today’s Episode

Hello and welcome to Interactive Biology TV, where we’re making biology fun! My name is Leslie Samuel, as usual. In this episode, Episode 11, we’re going to be talking about the last phase of the action potential, and that’s called hyperpolarization. If you watched the previous two episodes, we spoke about the first two phases, depolarization and repolarization. Now we’re talking about the last phase, hyperpolarization. Where we ended off in the last episode, potassium was rushing out of the cell, because voltage-gated potassium ion channels opened, and potassium wanted to leave, so potassium is now gone.

Now, potassium, as it’s going out of the cell, it’s trying to reach its equilibrium potential, which is somewhere around -93 millivolts. The resting membrane potential is somewhere around -70 millivolts, so we’re going lower than that resting membrane potential, and that process is called hyperpolarization. In other words, it’s over-polarized. It’s overshooting the resting membrane potential and going even more negative towards the equilibrium potential for potassium, because that’s where potassium wants to be.

Now, once we start heading towards that really negative -93 millivolts, there’s another process that’s still happening in the background, and that’s the sodium-potassium pump. It’s still doing its work. If you remember what that is, from the episode where we talked about the channels in the membrane, the proteins in the membrane, the sodium-potassium pump pumps 3 sodium ions out, and it pumps 2 potassium ions in. What that does as it’s working is it brings that membrane potential right back around the resting membrane potential. That’s the end of the action potential.

So we have depolarization, repolarization, hyperpolarization, and then the sodium-potassium pump doing its job to bring it back to resting situations. That’s it for this video, and if you have questions, you can go ahead and leave them in the comments below. I’ll be happy to take a look at those and maybe even answer it in a video like this. That’s all for this video, and I’ll see you in the next one.

http://www.youtube.com/watch?v=xmn0Vcd_wLA

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Ok, so by now you should have an understanding of Depolarization: Phase 1 of the Action Potential. If not, then what are you doing here? Don’t watch this video as yet. Check out the previous video first

Now your ready to learn about Phase 2, which is Repolarization. If you need a refresher on what an Action potential is, check out the episode entitled What is and Action Potential.

If you have any questions, leave them below. Enjoy!

- Leslie Samuel

Transcript of Today’s Episode

Hello and welcome to Interactive Biology TV. My name is Leslie Samuel. In this episode, we’re going to be talking about repolarization, which is the second phase of the action potential. Now, if you haven’t watched Episode 9 as yet, stop this video right now and go back to Episode 9. Watch that first, and then watch this second, because this is the second phase of the action potential.

Now, in the first phase, we said sodium rushed in, making the membrane potential more positive because the voltage-gated sodium channels open. Now, you’re going to see a little addition to the set-up, the “Action Potential Simulator” that we had, and you’ll see we have these blue marbles. These blue marbles are to represent potassium ions, or K+. These potassium ions also have a positive charge.

Now, we have all of these positive ions inside the cell, and we have so many potassium ions inside the cell that potassium wants to rush out. But once again, normally, potassium ions cannot just rush out. The voltage-gated potassium channels, which you can see here by this yellow divider, need to open first.

So, sodium rushed in, making the membrane potential very positive, relatively speaking. And because the membrane potential is that positive, that’s enough now to open these voltage-gated potassium channels. And what’s going to happen when the voltage-gated potassium channels open? Well, you guessed it. Potassium is going to do what it wants to do: it’s going to rush out. The equilibrium potential for potassium is negative, so it wants the charge across the membrane to be negative. So, by all of these potassium ions leaving, that makes the membrane potential more negative, and that process is called repolarization.

So first we had depolarization, now we have enough charge for the voltage-gated potassium channels to open. Once those open, potassium ions are going to rush out, making the membrane potential more negative. That’s the second phase of the action potential, repolarization.

If you have any questions about that, as usual, leave me a comment. I’ll be happy to answer your question, and maybe even make a video answering your specific question. That’s all for this video, and I’ll see you in the next one.

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

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The action potential can be a complicated thing to understand, unless you are dealing with little white plusses on a table

In this video, I help you visualize the first phase of the action potential – the Depolarization phase.

Go ahead and watch the video and you should get a clear understanding of the events that cause depolarization of the neuron.

- Leslie Samuel

Transcript of Today’s Video

Hello and welcome to Interactive Biology TV, where we’re making biology fun! In this episode, we’re going to be talking about depolarization, which is the first phase of the action potential. We’re going to go into some more detail than we’ve been doing in the past when it comes to the action potential. It’s going to be a little different. You’re not going to be looking at me talking about something. You’re actually going to be looking at another one of my elaborate set-ups, and I’m going to call this set-up the “Action Potential Simulator.” I hope that gets you excited about it.

Alright, so what we have here is, this side represents outside the cell, outside the axon, and this side represents inside the axon. Here we have a bunch of pluses, and these pluses are representing sodium ions. Now, sodium ions have a positive charge, and that’s why I chose these very attractive pluses to represent sodium ions.

Now, here in the center, we have what we’re going to refer to as voltage-gated sodium channels. What happens is, you have all these sodium ions on the outside of the cell, and these sodium ions want to get into the cell, but they cannot get into the cell. Why can’t they get into the cell? Because the voltage-gated sodium channels are closed. In order for them to get into the cell, this channel needs to open.

Now, why does sodium want to get into the cell? Well, if you go back to Episode 6, this can refresh your memory a little bit, we spoke about Donnan equilibrium. And we spoke about the fact that the membrane potential at rest is somewhere between -50 to -70, -80 millivolts. At that negative charge, sodium ions are not happy. In order for these guys to be happy, the membrane potential needs to be around +58. And on the inside of the cell, we have a negative charge, so this is not something that sodium likes.

So how does sodium want to counteract this? Well, sodium wants to rush into the cell so that it can make the membrane potential more positive, which will be closer to the Donnan equilibrium potential for sodium ions. I hope that makes sense, if not, once again, go back to Episode 6 and refresh your memory on how the Donnan equilibrium works.

So, someone touches you or there’s some stimulation and there needs to be an action potential that’s sent along the axons of the neurons that are stimulated. What happens is, when the membrane potential reaches threshold, that is enough charge to cause voltage-gated sodium channels to open. Once those voltage-gated sodium channels open, sodium ions can then go into the cell.

Now, what is this going to do to the charge inside the cell? What is it going to do to the membrane potential? Well, now you see you have all these positives on the inside, so that’s going to make the membrane potential more positive. This is the process of depolarization. It is the first phase of the action potential, and this is how the charge starts that gets sent along the axon.

So once again, when the membrane potential reaches threshold, voltage-gated sodium channels open and once those open, sodium ions are going to rush into the cell, making the membrane potential more positive, and that is depolarization. I hope that makes sense to you. If you have any questions, as usual, feel free to ask them in the comments below, and I’ll be happy to answer your questions. And who knows, maybe even make a video answering your specific question. That’s it for this video, and I’ll see you in the next one.

http://www.youtube.com/watch?v=4M1zzT9J_y4

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Ever wondered why people refer to the action potential as “all-or-none”?

Well, I guess you’ll just have to watch the video above to understand. In this video, I use the kitchen sink, a paper towel and marbles to bring the concept home.

If you have any questions/comments, feel free to leave it in the comments field below.

- Leslie Samuel

Transcript of Today’s Video

Hey, this is Leslie Samuel again and I’m kind of excited today. I just posted a poll on my blog, and it was for you guys to help me to decide what the subtitle or slogan for Interactive Biology will be, and the one that you guys decided on was “Making biology fun.” So this is the first time I get to use this introduction. Are you ready for it?

Hello and welcome to Interactive Biology TV, where we’re making biology fun! I like the ring of that. I wasn’t going for that title before, but when you guys suggested it, when you guys voted on it, it really started getting me excited.

Anyhow, in today’s episode, we’re going to be talking about the all-or-none nature of the action potential. We’ve been talking about the nervous system, and depending on which book you read, it might say “all-or-none” or “all-or-nothing.” Either way, we’re talking about the same thing. Now, there are two terms that I want you to know for this episode. The first one is the axon hillock, and the second would be the threshold, okay? We’re in my kitchen today, and I’m going to be using a high-tech device to illustrate these concepts. So, let’s look at what we have here today.

Alright, so this is my high-tech device for today. I’m not going to be doing any dishes even though we’re by the sink, but hopefully, this will get you guys to understand the concept of the all-or-none nature of the action potential. So the two terms I said were the axon hillock and the threshold. Axon hillock is the place where the axon starts. We looked at the neuron and the parts of the neuron, and right where it goes from the soma to the axon, we have the axon hillock. That’s the first place we see voltage-gated ion channels. In a previous episode, I spoke about the proteins in the membrane, and you can go back to that and see what these voltage-gated ion channels do.

But anyhow, this is where action potentials can start. However, in order for them to start, the stimulation needs to be enough to bring it to the threshold. So this, we’re going to imagine that this is my axon hillock, and in order for an action potential to happen, this needs to break, and when this breaks, voltage-gated channels open and ions rush in, and we have that electrical signal.

So, these are my ions, the little blue marbles, and I’m going to put the first one on here and nothing happens, that’s not enough to cause an action potential. I’ll put the second one and nothing happens. This is a pretty strong piece of paper towel. It’s Brawny, and I think that’s the one where you see a really strong man on the plastic wrap, so that should say something about the strength, I think.

Anyhow, I’m going to continue putting, still no action potential. It has not reached threshold just yet, so I’m just going to continue putting these ions. I’m trying to bring it to threshold, but it’s not there as yet. And we’re going to put some more. Evidently, Brawny is pretty strong. No insult against Bounty or any of those other paper towels. But here we go, I’m going to continue putting more stimulation, more stimulation, nothing happens. It’s pretty strong, so let’s dump some more on there. At a certain point, it’s going to reach a point where…

Oh! There we go . . . it breaks and those ions get through. That point was the threshold. Now, up until that point, nothing happened. But once we reached that point, we reached the threshold, it’s enough stimulus to cause the action potential to happen. That is why we call it all-or-none.

So there you have it, it’s all-or-none. It’s either going to happen or it’s not going to happen. If there’s enough stimulation to reach the threshold, as you saw with this elaborate set-up, if there’s enough stimulation, it will cause an action potential. If there isn’t enough, it will not cause an action potential. That’s why we call it all-or-nothing, all-or-none. I hope you enjoyed this episode. If you have any questions or comments, leave them in the comments field below. I’d be happy to answer your questions. Who knows, I might even make a video to answer your specific question. That’s it for this video, and I’ll see you in the next one.

http://www.youtube.com/watch?v=POSPO8QbZI4

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What is an Action Potential?

That’s the question I’m answering in todays Interactive Biology Episode. Watch the video above to find out

This is the first in my new video format and I really hope you enjoy it.

Once you have finished watching the video, go ahead and leave your comments below.

If you have any questions, that would be the place to ask them.

- Leslie Samuel

Transcript Of Today’s Video

Welcome to another episode of Interactive Biology TV. My name is Leslie Samuel. In this video, I’m going to be answering one basic question: What is an action potential? You’re probably going to notice that it’s a little different than the 6 episodes that I’ve done before. And the 2 main differences that you’re going to notice are:

1. I no longer call it BioVid. The reason for that is “Biovid” doesn’t really tell what this is all about. I’ve changed it to Interactive Biology TV, because it’s going to be interactive, it’s going to be about biology, and it’s going to be a video. So from now on, you’re going to hear me say “Interactive Biology TV” as opposed to “BioVid.”
2. You’re going to notice that I’m on camera this time, and that’s a little different because in the past, I’ve done slides and animations and so on. The reason I’m making this change is basically because I wanted to do something that I can produce much quickly. In the last year, I only made 6 episodes, and I want to be doing episodes on a regular basis and this is just easier for me to produce and I can put together a relatively professional-quality video in a short period of time.

I hope you enjoy this new format. Please let me know in the comments below, and if you have questions or comments about it, you can just do that. It’s going to be relatively laid-back and I’m just going to be talking to you about these different concepts.

So, let’s get into the content for today. Today, I’m answering the question “What is an action potential?” If you’ve looked at any of the previous episodes, you’ve seen that I’ve given an introduction to the nervous system and to neurons. That introduction to neurons basically comes right before this in terms of understanding the concepts, the different parts of the neuron.

Now, the main part of the neuron that we’re going to be talking about today is the axon. I have a very amazing device here that I’m going to be using to illustrate that. The axon is the part that sends the signal. A signal starts in the soma, there’s processing that happens in the soma, and we’re going to talk about that later on. It sends a signal via the axon, to the ends of the axon, the axon terminals, and then that signal can basically go to the next neuron.

How I’m going to illustrate this is really simple. If someone touches your hand, you feel it. And the reason you feel it is because there are signals that start at that point, and the signals go to your spinal cord, and then up to your brain. These are electrical signals that happen relatively quickly, so that your brain can interpret that stimulation, and your brain tells you “Okay, someone is touching you.”

That is an action potential. You can call it an action potential, you can also call it a nerve impulse, but it’s basically that electrical signal that goes from that stimulation point all the way to the brain. And these signals are going on throughout the body, doing a bunch of different things, and we’re going to talk about that.

So, here we have my handy-dandy iPhone 4. I’m going to turn it on. And I have my earbuds, I’m going to put these on. I’m assuming you guys know how this works, but the iPhone 4 is an amazing device. It has built-in an iPod, and I’m going to assume you know what an iPod is. You know what, I’m going to tell you what an iPod is, just for some strange reason you don’t know what an that is. It’s an MP3 player that allows you to play music and audio books and a whole bunch of other stuff.

Anyhow, I’m going to stimulate this iPhone, and it’s going to send an electrical signal via this cable to the earbuds, and we’re going to assume as if it’s going to my brain. And it is going to my brain. So, here we have a cable sending signals, and then there can be a response. The brain can interpret that stimulation. Okay, so I’m going to press Play, and this is me stimulating. And as soon as I press Play, I can hear music. I can dance to the music, I can do a whole bunch of stuff. Let me stop that for now.

But basically, here we have that wire, and these are the axons of the neurons sending signals to the brain, to different parts of the body. It’s basically how the nervous system communicates with the different cells and organs and the glands. So, really simple, the action potential is that signal that goes through the axons along the nerves and basically takes a signal from one place to another place, whether that’s from the brain to my hand that pulls away, whether it’s from the stimulation point all the way to my brain.

I hope that makes sense for you. That’s basically what an action potential is. If you have any questions, comments, leave it below in the comments field. I’d be happy to follow up and answer your questions, or even make a video about it. That’s it for this episode, and I’ll see you on the next one.

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Watch Donnan Equilibrium and Driving Force on Youtube

]]> http://www.interactive-biology.com/956/donnan-equilibrium-and-driving-force/feed/ 24 http://www.interactive-biology.com/901/the-isoelectric-point-of-proteins/ http://www.interactive-biology.com/901/the-isoelectric-point-of-proteins/#comments Sun, 18 Jul 2010 20:32:18 +0000 Leslie Samuel http://www.interactive-biology.com/?p=901 In this video, I talk about the isoelectric points of the proteins inside the neuron and how that results in the proteins having a negative charge. Understanding the negative charge of proteins inside the cell is important to understanding how neurons function. In the video, I also talk about the pH inside the cell. Just as a brief reminder, the pH tells how acidic or basic a solution is. If you need more info on pH, check out what Wikipedia has to say about pH.

There are 4 important classes of proteins in the membrane of neurons: Passive/Leakage ion channels, Sodium-Potassium pumps, Voltage-gated ion channels, and Ligand-gated ion channels. In order to understand how the neurons functions, we have to understand how those channels work. Watch the following video to learn about these proteins.

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Click Here to Download This Video

An Introduction to Neurons (Watch on Youtube)

In this Episode, I give an Introduction to neurons. Since Neurons form the basis for the entire Nervous System, understanding what they are and what they do is essential.

First I answer the question “What is a neuron?”. Then I go into the parts of a neuron:

• Dendrites
• Soma
• Axon
• Axon Terminals

Lastly, I talk about the three types of neurons:

• Sensory Neurons
• Motor Neurons
• Interneurons

Watch, Enjoy, and then leave your comments. There are many more videos to come. My goal is to provide at least 1 new Video on a weekly basis, so keep checking back.

This is the first in my series of BioVid Episodes: Video Tutorials to help with Biology. In the first section of my BioVid Tutorials, I will be dealing with The Nervous System. To start it all off, in this BioVid Episode, I give an introduction to the Nervous System. First, I answer the question “What is The Nervous System?”. Then I a talk about the two divisions of the Nervous System:

• Central Nervous System
• Peripheral Nervous System

Watch, Enjoy, and then leave your comments. There are many more videos to come. My goal is to provide at least 1 new Video on a weekly basis, so keep checking back.