February 8, 2011

031 How Rods and Cones Respond to Light

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.


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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