Light and Dark Adaptation

Hi Ninja Nerds, in this video we're going to talk about light and dark adaptation. So why is this important to talk about? You guys have probably all experienced this. Let's say that you guys went to go watch a movie. Alright, you guys were in the dark watching this movie the whole time. Then you guys decided, okay I'm going to go outside now, the movie's over. And what happens? You walk outside and it's just like, ahhh! You get hit with a beam of white light, right? Because you're going from the dark to the light. Same thing could happen, let's say that you're actually going from light into a very, very dark room. Okay, so all the lights are off on your house, but for whatever, I'm sorry, all the lights on are on your house and you go from a really, really light room into a really, really dark room where you go down to the basement. Your eyes are constantly adjusting to the light and the dark. I want to talk about how that's happening. Okay, so let's go ahead and get started. So first off, where are we going to find these structures? If you guys watched our video on the phototransduction cascade, you'll know what these are basically called, right? We're going to call this bad boy here, we're going to call this, A rod. Okay? So this is called a rod. And then this sucker over here is called a cone. Okay? And if you remember, rods were basically important because these are photoreceptors. They consist of a chemical called rhodopsin. And then cones consist of a chemical called Photopsin. And if you remember, it has different Photopsins that response to different wavelengths of light. Specifically that around blue, green, and red. Which allows for us to have color vision and visual acuity. So now, I'm going to write down a term here. Rods are very important for our retinal. Sensitivity. So they are important for retinal sensitivity. Okay and again what was that for? More of the dim light vision, more being able to see within the dark. What kind of vision did we call that? We said that that was for scotopic vision. Okay for scotopic vision. Some of this will be a review of what we talked about in the phototransduction cascade. So cones, what are they very very very good for? Cones are very important for visual acuity. Okay so for visual acuity. So Very, very specific, precise, edge detecting vision. Okay, being able to determine the shapes of some object. Being able to determine whether or not it can actually, if it's square or if it's circular. Right? Being able to see color, so also color. So it's also important for color vision. Okay, so cones are good for color vision. They're also good for visual acuity. Now, we said, oh, and last thing, What kind of vision would you call this for visual acuity and color vision and bright vision and a lot of that stuff? This is called photopic vision. Photopic vision, right? Now, let's do the example that we said first. Let's say that we do going from a movie theater, which is really, really dark. Okay, you just watched whatever. You watched the new Spider-Man movie. And you're coming out. And you get hit with a beam of light. How, what's going to happen? Not only do you get blinded with a white glare of light, a lot of things happens. So let's go through this. This is called dark to light adaptation. Okay, so first thing, first thing that happens within this dark to light adaptation, you guys should notice this right away with any individual. Whenever you're going from a dark room into a light room, what happens to the pupils? They constrict. The first thing is that the pupils are going to constrict. I'll talk about why they do that in just a second. Next thing that's going to happen is, what do you see whenever you get hit with really, really bright lights? Initially, you might see a white glare. You might see a white glare. But what happens is, The reason why you have that white glare is because you're bleaching your photopigments. You're bleaching the photopigments. What do I mean by you're bleaching them? What, am I taking Clorox and pouring it on them? No, I'm not doing that. There's a specific mechanism. If you guys remember, we had what's called rhodopsin. Let's use the rod as an example here. Let's say that we had that rhodopsin, right? And if you remember, rhodopsin, when we hit it with light, right, what happened? It broke the rhodopsin down, right? Specifically, what was the rhodopsin in the form of originally? It was in 11-cis-retinol, which was bound with opsin. It was tightly bound with this protein called opsin, which is kind of like a G-protein coupled receptor. When we hit it with light, We hit this with light. What did we do? We switched it from 11-cis-retinal to all-trans, and then Opsin was released. So this gets converted into all-trans-retinal, and then Opsin gets released, okay? And he gets active, you know, it can activate the transducer proteins, which will go and activate phosphodiesterases. So this is like the bleaching event. where the actual rhodopsin is getting broken down into the all-trans retinal and opsin. Now what happens is you have special enzymes that can actually regenerate this. Okay, so this is the regeneration process. So special enzymes are functioning to regenerate this. But this regeneration can take a little bit of time. Okay, it can take a little bit of time. So when you get hit or blasted with really, really bright light and you were in a dark room, The rhodopsin starts getting broken down excessively. Not only just rhodopsin, but also the actual pigments within the cones. The photopsin. Okay, so this also would get broken down. Now, as this is getting broken down, something really weird happens. Let me explain. Come over here to the rod for a second. If you guys remember, we had this molecule right here. Let's say that this is our rhodopsin. And then what did we do? We hit this rhodopsin with light rays. Okay, so we hit it with photons. And then what did it do? It split the actual off here. You got the actual what? All transretinal formed. From what structure? 11 cis. Okay, retinal. It gets converted from 11-cis-retinalin to all-trans. Then what else gets released? Opsin. Opsin goes and activates a protein here called, what was that protein called if you guys remember? It was called transducin. And then this transducin Did what? It went and activated a special enzyme located on this like disquietal membrane here and this enzyme here was called phosphodiesterase and if you remember phosphodiesterase did what? and stimulates phosphodiesterase, he breaks down the cyclic GMP. And if he breaks that down, then these sodium and calcium channels can't function. And then sodium and calcium can't come in, right? Now, something really weird happens that as you have this consistent breakdown of rhodopsin whenever you're going from a dark to a light room, this rhodopsin starts getting broken down excessively. That transducin is like, frick this, I can't do this anymore, you guys are activating me too much. And he decides that he's gonna leave and he's gonna come into this segment here. Now, what is this segment here called? This segment here is called the inner segment. This is called the inner segment and this little ruffled part here is called the outer segment. So what happens? Whenever this light, you're going from a dark to a light room, transduction leaves and goes into the inner segment. So he's going to go into the inner segment to stay. If he goes into the inner segment to stay, then what happens? When transducin leaves, he's like, Frick this, can't do this anymore, I'm not going to do this. The rhodopsin, the rods are going to stop functioning. Because now even if you try to hit this rhodopsin with light, the rhodopsin is not going to respond because most of it is existing in the all-trans retinal form. Okay, we want to regenerate and bring it back to 11-cis. But if we keep hitting it with light, that's not going to happen. So because of this, because the transducin leaves, the rods turn off. So the rods... turn off during this dark to light adaptation. Okay, so what happens to the retinal sensitivity? It decreases. So the retinal sensitivity will decrease. What does that mean? That means your scotopic vision is going to be decreasing. So that means that you're not going to be very good at being able to see dim light or fuzzy light or different shades of gray. Then who comes to the rescue? Cones. Some of the cones within your retina. Where exactly? In the retina would you find these? Let's imagine for a second. I take and I slice the eyeball and I'm going to look in the back of the eyeball. In the back of the eyeball here, this is the back of the eyeball. You see this structure right here that I'm drawing in blue? This is the optic nerve. That's where it actually is going to pierce through the back of the sclera. But we don't really call it that. We call it the optic disc or the blind spot. A little bit more outside from that is going to be this nice pink structure here. This is called the macula lutea and lutea means yellow and inside of this right in the center of it is going to be this special structure in here. There's a special structure in here and that special structure in there is called the fovea centralis. So inside of the macula lutea you have a structure here called the fovea centralis. The fovea centralis is where the highest concentration of cones are at. Okay? Okay, so you know where most of the cones are located. They're pretty much located within the macula lutea or inside of the fovea centralis. Where's the rods located? The rods are more located on the peripheral parts of the retina. So imagine all this that I'm kind of like drawing within this like baby bluish color here. All this out here is going to be rods. So you can get that we have more rods than we do cones. So first off, you're going to notice two things. First off, you're going to notice that there's going to be more rods than there are cones. And you're going to notice that the rods are more located within the periphery, whereas the cones are located within the center. Okay? There's an importance to that, and we'll talk about that. Okay? So these are your rods. So now, what do we know then? We know that rods, there's going to be more rods than there is cones. Okay, so we can even rewrite it like this. Rods, we know that there's going to be more of them than cones. And then we also know that the rods are located in periphery. Okay? Okay, so the rods are located within the periphery, whereas the cones are very, very concentrated or centrally located within the fovea centralis, within the macula lutea. Alright? Okay. Why is that important? Okay, so let's say that you're going from a dark area to a light area. What did we say happens? Your pupils constrict. If your pupils constrict, come over here for a second. Let's say right here. Let's put right here. Let's make that the macula. Let's actually kind of put a little bit more over here. A little bit more about right here. Now that's the macula and we constrict the pupil. I constrict the pupil. Then what's going to happen? I'm going to focus more of the light rays in the center of the eye. Okay? So more of the light rays that are coming in here now are going to be centered onto a specific structure. What is that structure called? It's called the macula. What is in the center? of the macula, the foveus and trallus. And what is the foveus and trallus primarily made up of? Cones. So whenever you're going from a dark area to a light area, the pupils constrict so they can focus the light specifically onto what? Onto the retina. That's why the pupils constrict. So the pupils constrict to focus light centrally on macula. Okay, lutea, which is where the fovea centralis is. That's where the highest concentration of cones are. Okay, that should make sense. So first off, what has happened so far? Pupils constricted so that we could focus the light specifically on to the center of the macula lutea where the fovea centralis is, where the highest concentration of cones are. We're bleaching the photopigments very, very rapidly because we're getting hit with a lot of light at once. The rhodopsin is getting broken down continuously. Because the rhodopsin is getting broken down continuously, what happens to the rods? The rods turn off. Then, what happens then to the retinal sensitivity? Retinal sensitivity for the dim light or the fuzzy light or the different shades of gray kind of light, the retinal sensitivity decreases. What structures turn on? The cones turn on. And as the cones turn on, the less sensitive cones to the actual bright lights, the less sensitive cones, as those cones turn on, then what happens to the visual acuity? The visual acuity increases. And so does your color vision. And then what type of vision is going to be occurring at this point in time? Photopic vision. Now, if you guys have noticed, you go from a dark room to a light room, it's not going to happen immediately. It takes a little bit of time. Sometimes it can take about five to ten minutes, right? So, for this event it might take about five to ten minutes for your eyes to completely and perfectly adjust okay from going from a dark room into a light area all right so again to put that all out just to review it so without confused pupils constrict to focus the light on Onto the macula, where the highest concentration of cones are, where the fovea centralis is. Because of the light hitting it, from going into this dark to very, very bright light, the rods were pretty active, but now they're going to get bleached, so the rhodopsin is going to get excessively broken down, and where's transducin going to go? It's going to go to the inner segment. So even if light is hitting, rhodopsin can be broken down to generate some of those activities. So then, if that happens, and even some of the photopsin is broken down in the higher, like more sensitive cones. And then again, because the rhodopsin is excessively broken down and transducing goes into the inner segment, the rods turn off, retinal sensitivity decreases, and then the less sensitive cones are going to turn on. And their visual acuity increases and the color vision becomes very precise and that might take about 5 to 10 minutes. So that covers that. That covers the dark to light. Now, let's say that you're like, oh man, you know what? Spider-Man movie was so great. I'm going to go back in again and watch it again. Okay? Now what happens? Alright? So you say, alright I'm going to go back in and watch that movie again. So now we got to talk about light to dark adaptation. And it's pretty much just the reversal so it's not really going to be that confusing. It's just going to be the exact opposite of everything we did over there. So the first thing that's going to happen is when you go from a light room to a dark room, what happens to the pupils? The pupil should dilate. Okay, so now that we have a good understanding of what we see within the back of the retina, this pupil dilation should make a lot of sense. So now let's put our macula right here and again what's going to be within the center of the macula? You're going to have the foveus and tralus where the highest concentration of cones are. And then again spread out all around the retina here is going to be the? Rods here, right? And again this part right here I actually should get rid of and the reason why this is the optic disc So really there is no photoreceptors there now We dilate the pupils if we dilate the pupils, let's make these soccers huge. Okay, look at this These pupils are freaking huge. Now look what happens. All the light rays that are coming in can spread out to all different parts of the retina. So not only can the light hit this actual macula, but the light can hit the what? The outer peripheral parts. If you can hit the outer peripheral parts, which photoreceptors are going to be activated now? The rods. Okay, so you're going to be hitting a lot of rods. So now because of the dilation of the pupil. So pupils dilate. If the pupils dilate, what is that going to do? It's going to allow more light Into eye, reaching periphery of eye. And which parts are there? What is in the periphery of the eye? The rods. Okay? So we're going to be able to hit some more of that light on the rods instead of completely focusing on onto the macula lutea, where the fovea centralis is. That's the first thing. Second thing. Transducin is like, alright, you know what, I'll make a truce, I'll come back. So rhodopsin starts accumulating again. Okay, because what happens is this takes a little bit of time. This is not as fast as going from dark to light. If you guys have ever noticed that. It takes a while for your eyes to get adjusted going from a light to a dark room. It takes a little bit, it's not easy. So it does take a little bit and that's because this rhodopsin has to accumulate a little bit. So now what happens is, transducin that was out here in the inner segment, he comes back up. He comes back out to the outer segment. And as he does that, it allows for this accumulation of the rhodopsin again. So now the rhodopsin is sensitive to the light again, okay? This dim light, this dark light, the different shades of gray type of light. So now that the rhodopsin accumulates, it's now going to be sensitive to the light now. So now what happens to the retinal sensitivity for this dim light or fuzzy light or different shades of gray type of light? The retinal sensitivity will increase. Alright, now the rhodopsin accumulates because the transducin comes back. As the rhodopsin accumulates, it becomes more sensitive to the light. And whenever it's sensitive to the light, then whenever the light hits the rhodopsin, In the dim light or the fuzzy light, it can initiate this type of cascade event that will allow for the activation of these rods, right? Now, so the rods are going to be turned on. So rods turn on in this case. Third thing that's going to happen. Now the cones. The cones are going to get turned off. Here's why. The cones have a certain threshold of wavelength that they like to be hit with. Dark light is a low wavelength, okay? So low wavelength of lights aren't going to be really activating these cones. So because this low wavelength of light, it's not going to not... activate cones. Okay, so because the light intensity, okay, we could even say this, there's besides the decreasing wavelength, we can say decreased light intensity. So as the intensity of light decreases, it doesn't activate the cones, the photopsins much. So they get turned off. So now what happens to the visual acuity? The visual acuity Well, decrease. What happens to the color vision? Decrease in color vision. Okay, now I'm talking a complete dark room. Obviously, if you go back in to watch a movie, there will be the lights and all that stuff like that. But just imagine going from a very bright room into a dark room. Okay, turn all the lights off in your house instantly. Let's say it's dark. at night, it's nine o'clock at night, you're going to bed and you were in a bright light room and you shut the lights off immediately. Boom. Complete pitch black. You can't see anything. Why? Because your rhodopsin has to start accumulating. That's why I said it takes a little bit more time. And it might take a while before you start seeing anything. So the rhodopsin has to start accumulating. And when it starts accumulating, The retina sensitivity will increase and then the rods will finally turn on. What else happens? The pupils dilate so that more light hits the periphery to activate those rods because your rods are for your scotopic vision, your dim light vision, the fuzzy vision, for different shades of gray. Then, our cones turn off because they're not going to respond to that decreased light intensity from the dim light. Okay, now if you notice, if it's complete pitch black, would I be able to notice the color of this marker or the shape of this marker that well? No, not as much as I would be able to notice it in this light. In darkness, I might not be able to see that very well. So I might not be able to see the color that well and I might not be able to see the actual complete shape of it perfectly. So that's what's going to happen during the actual going from this light to dark adaptation. This takes a little bit longer. This could actually take up, in certain situations, on average, about 20 to 30 minutes, okay, for this light to dark adaptation to occur, okay? All right, last thing, guys, to finish up. Cones. You know, there's a certain situation, you know, it controls your photopic vision or your color vision. You guys have probably heard of color blindness. Well, color blindness is actually an X-linked. Recessive disorder usually. Okay, so it's usually an X-linked recessive disorder. So it's again it's going to be more common within the males right and in this situation what can happen is you're actually going to be lacking certain types of photopsins and usually the most common types of photopsins that are affected is going to be that of the red okay that are responding to the red wavelengths. as well as those responding to the green wavelengths. So this is the red-green color blindness, where they have a hard time being able to see red and green within the different shades, right? So that's a hard thing there for some of these people. So they might have certain types of X-linked recessive disorders where their actual photopsins are completely mutated or deficient, where they don't produce the actual photopsins to respond to red wavelengths of light or green wavelengths of light. All right. And that can cause the color blindness. All right. Another thing, what if people don't ever adapt? They can't ever see anything in the dark. So you go from a light and then you go into dark and they never adapt. They never form anything that they can actually see at all. Complete pitch black. They never adjust. This is a terrible condition. And this is called nyctalopia. Nyctalopia or night blindness. Okay, this is usually due to a decrease in the production of vitamin A or decrease Intake of vitamin A because if you remember I talked about this in the photo transduction cascade Vitamin A is actually oxidized remember we remove off the two protons and we convert this into Retin-L specifically like the 11 sis form right now if I have a decreased vitamin I'm gonna make less retinol and I'm gonna be able to I'm not gonna be able to respond to light as much right because remember 11 sis retina has to get converted into all Trans right now and then it has to get regenerated back into this but again vitamin A is feeding into this So if there's a decrease in vitamin A there's a decrease in the photopigments So you're not gonna be able to respond to the actual dim light because you're not gonna have as many of them Oh, and then there's another one That's actually affecting this. It's called retinitis pigmentosa. Retinitis pigmentosa. This is actually another situation here. You know, if you guys remember from the phototransduction cascade, we had these cells back here, the pigmented epithelium, which was rich in melanin, and they were basically helpful for being able to absorb. any scattering light rays or provide nutrients and blood flow to the actual photoreceptors. And what was another thing it was doing? Remember the rods? It was recycling a lot of the tips from them that were actually coming off. It was phagocytosing it and recycling it. In retinitis pigmentosa, they're not able to recycle and phagocytose these actual tips from the rods. If they can't phagocytose these actual tips and then recycle them, what happens to the actual rods then? They start degenerating. As the rods degenerate, Do you think these people are going to be able to see well at night? No. And again, this could actually cause this actual night blindness also. Okay. All right, Ninja Nerds. In this video, we did a lot of information about light and dark adaptation. We talked through just a little bit of clinical correlation in that. I hope all of it made sense. I hope you guys really did enjoy it. If you guys did, please hit the like button, comment down in the comment section, and please subscribe. As always, Ninja Nerds, until next time.

Hi Ninja Nerds, in this video we're going to talk about light and dark adaptation. So why is this important to talk about? You guys have probably all experienced this.

Let's say that you guys went to go watch a movie. Alright, you guys were in the dark watching this movie the whole time. Then you guys decided, okay I'm going to go outside now, the movie's over. And what happens?

You walk outside and it's just like, ahhh! You get hit with a beam of white light, right? Because you're going from the dark to the light. Same thing could happen, let's say that you're actually going from light into a very, very dark room. Okay, so all the lights are off on your house, but for whatever, I'm sorry, all the lights on are on your house and you go from a really, really light room into a really, really dark room where you go down to the basement.

Your eyes are constantly adjusting to the light and the dark. I want to talk about how that's happening. Okay, so let's go ahead and get started. So first off, where are we going to find these structures? If you guys watched our video on the phototransduction cascade, you'll know what these are basically called, right?

We're going to call this bad boy here, we're going to call this, A rod. Okay? So this is called a rod. And then this sucker over here is called a cone. Okay?

And if you remember, rods were basically important because these are photoreceptors. They consist of a chemical called rhodopsin. And then cones consist of a chemical called Photopsin.

And if you remember, it has different Photopsins that response to different wavelengths of light. Specifically that around blue, green, and red. Which allows for us to have color vision and visual acuity.

So now, I'm going to write down a term here. Rods are very important for our retinal. Sensitivity. So they are important for retinal sensitivity. Okay and again what was that for?

More of the dim light vision, more being able to see within the dark. What kind of vision did we call that? We said that that was for scotopic vision.

Okay for scotopic vision. Some of this will be a review of what we talked about in the phototransduction cascade. So cones, what are they very very very good for? Cones are very important for visual acuity. Okay so for visual acuity.

So Very, very specific, precise, edge detecting vision. Okay, being able to determine the shapes of some object. Being able to determine whether or not it can actually, if it's square or if it's circular. Right?

Being able to see color, so also color. So it's also important for color vision. Okay, so cones are good for color vision.

They're also good for visual acuity. Now, we said, oh, and last thing, What kind of vision would you call this for visual acuity and color vision and bright vision and a lot of that stuff? This is called photopic vision. Photopic vision, right?

Now, let's do the example that we said first. Let's say that we do going from a movie theater, which is really, really dark. Okay, you just watched whatever.

You watched the new Spider-Man movie. And you're coming out. And you get hit with a beam of light.

How, what's going to happen? Not only do you get blinded with a white glare of light, a lot of things happens. So let's go through this.

This is called dark to light adaptation. Okay, so first thing, first thing that happens within this dark to light adaptation, you guys should notice this right away with any individual. Whenever you're going from a dark room into a light room, what happens to the pupils? They constrict.

The first thing is that the pupils are going to constrict. I'll talk about why they do that in just a second. Next thing that's going to happen is, what do you see whenever you get hit with really, really bright lights? Initially, you might see a white glare. You might see a white glare.

But what happens is, The reason why you have that white glare is because you're bleaching your photopigments. You're bleaching the photopigments. What do I mean by you're bleaching them? What, am I taking Clorox and pouring it on them? No, I'm not doing that.

There's a specific mechanism. If you guys remember, we had what's called rhodopsin. Let's use the rod as an example here.

Let's say that we had that rhodopsin, right? And if you remember, rhodopsin, when we hit it with light, right, what happened? It broke the rhodopsin down, right?

Specifically, what was the rhodopsin in the form of originally? It was in 11-cis-retinol, which was bound with opsin. It was tightly bound with this protein called opsin, which is kind of like a G-protein coupled receptor. When we hit it with light, We hit this with light.

What did we do? We switched it from 11-cis-retinal to all-trans, and then Opsin was released. So this gets converted into all-trans-retinal, and then Opsin gets released, okay?

And he gets active, you know, it can activate the transducer proteins, which will go and activate phosphodiesterases. So this is like the bleaching event. where the actual rhodopsin is getting broken down into the all-trans retinal and opsin.

Now what happens is you have special enzymes that can actually regenerate this. Okay, so this is the regeneration process. So special enzymes are functioning to regenerate this. But this regeneration can take a little bit of time.

Okay, it can take a little bit of time. So when you get hit or blasted with really, really bright light and you were in a dark room, The rhodopsin starts getting broken down excessively. Not only just rhodopsin, but also the actual pigments within the cones.

The photopsin. Okay, so this also would get broken down. Now, as this is getting broken down, something really weird happens.

Let me explain. Come over here to the rod for a second. If you guys remember, we had this molecule right here. Let's say that this is our rhodopsin.

And then what did we do? We hit this rhodopsin with light rays. Okay, so we hit it with photons. And then what did it do? It split the actual off here.

You got the actual what? All transretinal formed. From what structure? 11 cis.

Okay, retinal. It gets converted from 11-cis-retinalin to all-trans. Then what else gets released? Opsin. Opsin goes and activates a protein here called, what was that protein called if you guys remember?

It was called transducin. And then this transducin Did what? It went and activated a special enzyme located on this like disquietal membrane here and this enzyme here was called phosphodiesterase and if you remember phosphodiesterase did what?

and stimulates phosphodiesterase, he breaks down the cyclic GMP. And if he breaks that down, then these sodium and calcium channels can't function. And then sodium and calcium can't come in, right?

Now, something really weird happens that as you have this consistent breakdown of rhodopsin whenever you're going from a dark to a light room, this rhodopsin starts getting broken down excessively. That transducin is like, frick this, I can't do this anymore, you guys are activating me too much. And he decides that he's gonna leave and he's gonna come into this segment here.

Now, what is this segment here called? This segment here is called the inner segment. This is called the inner segment and this little ruffled part here is called the outer segment.

So what happens? Whenever this light, you're going from a dark to a light room, transduction leaves and goes into the inner segment. So he's going to go into the inner segment to stay.

If he goes into the inner segment to stay, then what happens? When transducin leaves, he's like, Frick this, can't do this anymore, I'm not going to do this. The rhodopsin, the rods are going to stop functioning. Because now even if you try to hit this rhodopsin with light, the rhodopsin is not going to respond because most of it is existing in the all-trans retinal form.

Okay, we want to regenerate and bring it back to 11-cis. But if we keep hitting it with light, that's not going to happen. So because of this, because the transducin leaves, the rods turn off. So the rods...

turn off during this dark to light adaptation. Okay, so what happens to the retinal sensitivity? It decreases.

So the retinal sensitivity will decrease. What does that mean? That means your scotopic vision is going to be decreasing. So that means that you're not going to be very good at being able to see dim light or fuzzy light or different shades of gray.

Then who comes to the rescue? Cones. Some of the cones within your retina. Where exactly?

In the retina would you find these? Let's imagine for a second. I take and I slice the eyeball and I'm going to look in the back of the eyeball. In the back of the eyeball here, this is the back of the eyeball.

You see this structure right here that I'm drawing in blue? This is the optic nerve. That's where it actually is going to pierce through the back of the sclera.

But we don't really call it that. We call it the optic disc or the blind spot. A little bit more outside from that is going to be this nice pink structure here. This is called the macula lutea and lutea means yellow and inside of this right in the center of it is going to be this special structure in here.

There's a special structure in here and that special structure in there is called the fovea centralis. So inside of the macula lutea you have a structure here called the fovea centralis. The fovea centralis is where the highest concentration of cones are at. Okay? Okay, so you know where most of the cones are located.

They're pretty much located within the macula lutea or inside of the fovea centralis. Where's the rods located? The rods are more located on the peripheral parts of the retina. So imagine all this that I'm kind of like drawing within this like baby bluish color here.

All this out here is going to be rods. So you can get that we have more rods than we do cones. So first off, you're going to notice two things.

First off, you're going to notice that there's going to be more rods than there are cones. And you're going to notice that the rods are more located within the periphery, whereas the cones are located within the center. Okay?

There's an importance to that, and we'll talk about that. Okay? So these are your rods. So now, what do we know then? We know that rods, there's going to be more rods than there is cones.

Okay, so we can even rewrite it like this. Rods, we know that there's going to be more of them than cones. And then we also know that the rods are located in periphery.

Okay? Okay, so the rods are located within the periphery, whereas the cones are very, very concentrated or centrally located within the fovea centralis, within the macula lutea. Alright? Okay.

Why is that important? Okay, so let's say that you're going from a dark area to a light area. What did we say happens?

Your pupils constrict. If your pupils constrict, come over here for a second. Let's say right here. Let's put right here. Let's make that the macula.

Let's actually kind of put a little bit more over here. A little bit more about right here. Now that's the macula and we constrict the pupil.

I constrict the pupil. Then what's going to happen? I'm going to focus more of the light rays in the center of the eye.

Okay? So more of the light rays that are coming in here now are going to be centered onto a specific structure. What is that structure called?

It's called the macula. What is in the center? of the macula, the foveus and trallus. And what is the foveus and trallus primarily made up of?

Cones. So whenever you're going from a dark area to a light area, the pupils constrict so they can focus the light specifically onto what? Onto the retina.

That's why the pupils constrict. So the pupils constrict to focus light centrally on macula. Okay, lutea, which is where the fovea centralis is. That's where the highest concentration of cones are.

Okay, that should make sense. So first off, what has happened so far? Pupils constricted so that we could focus the light specifically on to the center of the macula lutea where the fovea centralis is, where the highest concentration of cones are. We're bleaching the photopigments very, very rapidly because we're getting hit with a lot of light at once.

The rhodopsin is getting broken down continuously. Because the rhodopsin is getting broken down continuously, what happens to the rods? The rods turn off.

Then, what happens then to the retinal sensitivity? Retinal sensitivity for the dim light or the fuzzy light or the different shades of gray kind of light, the retinal sensitivity decreases. What structures turn on? The cones turn on.

And as the cones turn on, the less sensitive cones to the actual bright lights, the less sensitive cones, as those cones turn on, then what happens to the visual acuity? The visual acuity increases. And so does your color vision. And then what type of vision is going to be occurring at this point in time?

Photopic vision. Now, if you guys have noticed, you go from a dark room to a light room, it's not going to happen immediately. It takes a little bit of time.

Sometimes it can take about five to ten minutes, right? So, for this event it might take about five to ten minutes for your eyes to completely and perfectly adjust okay from going from a dark room into a light area all right so again to put that all out just to review it so without confused pupils constrict to focus the light on Onto the macula, where the highest concentration of cones are, where the fovea centralis is. Because of the light hitting it, from going into this dark to very, very bright light, the rods were pretty active, but now they're going to get bleached, so the rhodopsin is going to get excessively broken down, and where's transducin going to go?

It's going to go to the inner segment. So even if light is hitting, rhodopsin can be broken down to generate some of those activities. So then, if that happens, and even some of the photopsin is broken down in the higher, like more sensitive cones.

And then again, because the rhodopsin is excessively broken down and transducing goes into the inner segment, the rods turn off, retinal sensitivity decreases, and then the less sensitive cones are going to turn on. And their visual acuity increases and the color vision becomes very precise and that might take about 5 to 10 minutes. So that covers that. That covers the dark to light. Now, let's say that you're like, oh man, you know what?

Spider-Man movie was so great. I'm going to go back in again and watch it again. Okay? Now what happens?

Alright? So you say, alright I'm going to go back in and watch that movie again. So now we got to talk about light to dark adaptation.

And it's pretty much just the reversal so it's not really going to be that confusing. It's just going to be the exact opposite of everything we did over there. So the first thing that's going to happen is when you go from a light room to a dark room, what happens to the pupils?

The pupil should dilate. Okay, so now that we have a good understanding of what we see within the back of the retina, this pupil dilation should make a lot of sense. So now let's put our macula right here and again what's going to be within the center of the macula?

You're going to have the foveus and tralus where the highest concentration of cones are. And then again spread out all around the retina here is going to be the? Rods here, right?

And again this part right here I actually should get rid of and the reason why this is the optic disc So really there is no photoreceptors there now We dilate the pupils if we dilate the pupils, let's make these soccers huge. Okay, look at this These pupils are freaking huge. Now look what happens. All the light rays that are coming in can spread out to all different parts of the retina. So not only can the light hit this actual macula, but the light can hit the what?

The outer peripheral parts. If you can hit the outer peripheral parts, which photoreceptors are going to be activated now? The rods.

Okay, so you're going to be hitting a lot of rods. So now because of the dilation of the pupil. So pupils dilate. If the pupils dilate, what is that going to do?

It's going to allow more light Into eye, reaching periphery of eye. And which parts are there? What is in the periphery of the eye? The rods.

Okay? So we're going to be able to hit some more of that light on the rods instead of completely focusing on onto the macula lutea, where the fovea centralis is. That's the first thing.

Second thing. Transducin is like, alright, you know what, I'll make a truce, I'll come back. So rhodopsin starts accumulating again. Okay, because what happens is this takes a little bit of time. This is not as fast as going from dark to light.

If you guys have ever noticed that. It takes a while for your eyes to get adjusted going from a light to a dark room. It takes a little bit, it's not easy. So it does take a little bit and that's because this rhodopsin has to accumulate a little bit. So now what happens is, transducin that was out here in the inner segment, he comes back up.

He comes back out to the outer segment. And as he does that, it allows for this accumulation of the rhodopsin again. So now the rhodopsin is sensitive to the light again, okay? This dim light, this dark light, the different shades of gray type of light. So now that the rhodopsin accumulates, it's now going to be sensitive to the light now.

So now what happens to the retinal sensitivity for this dim light or fuzzy light or different shades of gray type of light? The retinal sensitivity will increase. Alright, now the rhodopsin accumulates because the transducin comes back. As the rhodopsin accumulates, it becomes more sensitive to the light. And whenever it's sensitive to the light, then whenever the light hits the rhodopsin, In the dim light or the fuzzy light, it can initiate this type of cascade event that will allow for the activation of these rods, right?

Now, so the rods are going to be turned on. So rods turn on in this case. Third thing that's going to happen. Now the cones. The cones are going to get turned off.

Here's why. The cones have a certain threshold of wavelength that they like to be hit with. Dark light is a low wavelength, okay?

So low wavelength of lights aren't going to be really activating these cones. So because this low wavelength of light, it's not going to not... activate cones. Okay, so because the light intensity, okay, we could even say this, there's besides the decreasing wavelength, we can say decreased light intensity. So as the intensity of light decreases, it doesn't activate the cones, the photopsins much.

So they get turned off. So now what happens to the visual acuity? The visual acuity Well, decrease.

What happens to the color vision? Decrease in color vision. Okay, now I'm talking a complete dark room.

Obviously, if you go back in to watch a movie, there will be the lights and all that stuff like that. But just imagine going from a very bright room into a dark room. Okay, turn all the lights off in your house instantly. Let's say it's dark.

at night, it's nine o'clock at night, you're going to bed and you were in a bright light room and you shut the lights off immediately. Boom. Complete pitch black.

You can't see anything. Why? Because your rhodopsin has to start accumulating.

That's why I said it takes a little bit more time. And it might take a while before you start seeing anything. So the rhodopsin has to start accumulating.

And when it starts accumulating, The retina sensitivity will increase and then the rods will finally turn on. What else happens? The pupils dilate so that more light hits the periphery to activate those rods because your rods are for your scotopic vision, your dim light vision, the fuzzy vision, for different shades of gray.

Then, our cones turn off because they're not going to respond to that decreased light intensity from the dim light. Okay, now if you notice, if it's complete pitch black, would I be able to notice the color of this marker or the shape of this marker that well? No, not as much as I would be able to notice it in this light. In darkness, I might not be able to see that very well.

So I might not be able to see the color that well and I might not be able to see the actual complete shape of it perfectly. So that's what's going to happen during the actual going from this light to dark adaptation. This takes a little bit longer.

This could actually take up, in certain situations, on average, about 20 to 30 minutes, okay, for this light to dark adaptation to occur, okay? All right, last thing, guys, to finish up. Cones. You know, there's a certain situation, you know, it controls your photopic vision or your color vision. You guys have probably heard of color blindness.

Well, color blindness is actually an X-linked. Recessive disorder usually. Okay, so it's usually an X-linked recessive disorder. So it's again it's going to be more common within the males right and in this situation what can happen is you're actually going to be lacking certain types of photopsins and usually the most common types of photopsins that are affected is going to be that of the red okay that are responding to the red wavelengths.

as well as those responding to the green wavelengths. So this is the red-green color blindness, where they have a hard time being able to see red and green within the different shades, right? So that's a hard thing there for some of these people. So they might have certain types of X-linked recessive disorders where their actual photopsins are completely mutated or deficient, where they don't produce the actual photopsins to respond to red wavelengths of light or green wavelengths of light. All right.

And that can cause the color blindness. All right. Another thing, what if people don't ever adapt?

They can't ever see anything in the dark. So you go from a light and then you go into dark and they never adapt. They never form anything that they can actually see at all. Complete pitch black. They never adjust.

This is a terrible condition. And this is called nyctalopia. Nyctalopia or night blindness.

Okay, this is usually due to a decrease in the production of vitamin A or decrease Intake of vitamin A because if you remember I talked about this in the photo transduction cascade Vitamin A is actually oxidized remember we remove off the two protons and we convert this into Retin-L specifically like the 11 sis form right now if I have a decreased vitamin I'm gonna make less retinol and I'm gonna be able to I'm not gonna be able to respond to light as much right because remember 11 sis retina has to get converted into all Trans right now and then it has to get regenerated back into this but again vitamin A is feeding into this So if there's a decrease in vitamin A there's a decrease in the photopigments So you're not gonna be able to respond to the actual dim light because you're not gonna have as many of them Oh, and then there's another one That's actually affecting this. It's called retinitis pigmentosa. Retinitis pigmentosa.

This is actually another situation here. You know, if you guys remember from the phototransduction cascade, we had these cells back here, the pigmented epithelium, which was rich in melanin, and they were basically helpful for being able to absorb. any scattering light rays or provide nutrients and blood flow to the actual photoreceptors.

And what was another thing it was doing? Remember the rods? It was recycling a lot of the tips from them that were actually coming off.

It was phagocytosing it and recycling it. In retinitis pigmentosa, they're not able to recycle and phagocytose these actual tips from the rods. If they can't phagocytose these actual tips and then recycle them, what happens to the actual rods then? They start degenerating.

As the rods degenerate, Do you think these people are going to be able to see well at night? No. And again, this could actually cause this actual night blindness also. Okay.

All right, Ninja Nerds. In this video, we did a lot of information about light and dark adaptation. We talked through just a little bit of clinical correlation in that.

I hope all of it made sense. I hope you guys really did enjoy it. If you guys did, please hit the like button, comment down in the comment section, and please subscribe.

As always, Ninja Nerds, until next time.

Transcript for:Light and Dark Adaptation

Transcript for:
Light and Dark Adaptation