In this video, we'll be talking about the special sense of vision. Specifically we'll be going into the anatomy of the eye and talk just a little bit about how the light-detecting cells in the eye are stimulated. There is a second video that will go into detail about phototransduction, how that stimulation of those light-detecting cells, how that stimulation is relayed back to the brain. For discussing the anatomy of the eye, we'll start with the muscles. There are two types of muscles that control responses in the eye-- you have the extrinsic muscles and the intrinsic muscles. The extrinsic muscles are those muscles that rotate the eyeball within its socket. So when the extrinsic muscles are active, they can cause lateral or medial movement of the iris and pupil, or they can cause elevation and depression. So if you're staring straight ahead, now look to the left, look to the right, look down-- you're using the extrinsic muscles of your eyes. The inferior rectus moves the eyeball to look inferiorly. The medial rectus, which isn't labeled on this diagram but you can see it back in there, the medial rectus turns the eyeball so that you look medially. The superior rectus turns the eyeball to look superiorly. The lateral rectus turns the eyeball to look laterally. The inferior oblique rolls the eyeball to look kind of superiorly and laterally, so like up into the upper-lateral corner. The superior oblique turns the eyeball, rolls the eyeball to look down and to the sides, so inferiorly and laterally. Notice that the way these muscles work together is that when you're looking to the left, you'll have different muscles active in each eye, because if you look to the left, your left eyeball is actually looking laterally, but your right eyeball is looking medially. So you'd need different muscles active in each eye. The intrinsic muscles are called intrinsic muscles because they're actually within the eyeball itself. And there are a couple of different types. So there are the ciliary muscles that are used to change the shape of the lens, and there are two sets of muscles that change the iris-- that are in the iris that change the size of the pupil, the opening that light passes through to enter into your eye. So the sphincter pupillae and the dilator pupillae. These muscles work together both in the response of your eyes to light and they work together to assist with focusing on objects. Now I want to get into the anatomy of the eyeball. There are three layers to the wall of the eye, so you can think of the eye as sort of like a jelly-filled ball. And there are three layers that form the ball, the outside of the eye. You have the fibrous layer, the vascular layer, and the sensory layer, and we'll talk about each of these in turn. The fibrous layer consists of the sclera and the cornea. The sclera is what makes your eyeballs white. It's a very tough tendon-like covering of the eye, kind of contains, holds, and provides some protection to everything inside the fibrous layer. But if you had a tendon sitting over the surface of your eye, you wouldn't be able to see much-- that's where the cornea comes in. The cornea is a transparent cap over your eye. So this layer basically becomes this transparent cornea over the anterior surface of the eye, allowing light to pass through the cornea, into the pupil, through the lens, and into the eyeball. The vascular layer is just deep to the fibrous layer. So the fibrous layer is this, the vascular layer is here. And the vascular layer is also called the uvea. There are a few different parts to the vascular layer. You have the chorold, which is highly vascularized. It's also pigmented, so it has coloration to it. And the choroid contains blood vessels that bring nutrients and oxygen to the wall of the eye. So much of the vascular layer is the chorold. Towards the anterior portion of the eye you find the ciliary body, and the ciliary body is smooth muscle fibers, so these are the ciliary muscles that we just discussed, one of the types of intrinsic muscles you find in the eye. And these smooth muscle fibers attach to the lens and they control the shape of the lens. Anterior to the ciliary body you have the iris, and the iris is the colored part of a visible eye. So if someone has blue eyes or brown eyes, it's because of the pigmentation of their iris. And the iris controls the size of the pupil. The pupil is basically a hole in the iris. And there are two smooth muscle layers in the iris that control the size of the pupil. There's circular muscle fibers that constrict the pupil and radial muscle fibers that dilate the pupil. This diagram shows how those muscles are arranged, and remember, we're talking smooth muscle fibers and how they control the size of the pupil. So here we have the circular muscle fibers, the pupillary constrictor, and then the radial muscle fibers, the pupillary dilator. So when these muscles are stimulated, they contract and they close down, reducing the size of the pupil. Like you see here, this happens when you have a bright light shone in your eye, you get parasympathetic stimulation of these circular muscles and your pupil will close down. And this also happens when you're focusing on close objects. It's part of what's called the accommodation reflex. We'll talk a little bit more about that, but it allows you to focus in on close objects by restricting the amount of light that gets into your eye. In contrast, when you're in dim light or when you have sympathetic stimulation happening, these pupillary dilator muscles get activated, and when they are activated and contract, they pull the pupil open so your pupils become dilated. Moving inward from the uvea, we have the retina, and the retina is the sensory layer. This is the layer of your eye that actually detects light. And there are two layers to the retinae. You have an outer pigmented epithelium and you have an inner neural layer. The neural layer contains the light-sensitive cells, and you have two types of light-sensitive cells-- the rods and the cones. You also have neuronal signaling cells - bipolar cells and ganglion cells - which are involved in relaying the light detection stimulus from the photoreceptors to the optic nerve and eventually to the brain. And I refer you again to the phototransduction video for a little bit more detail on that relay from photoreceptor to bipolar cells to ganglion cells. The optic nerve is basically a cluster of axons coming from the ganglion cells, and you actually have a blind spot in your eye where the optic nerve leaves the eye because these axons are leaving, you cannot have light-sensitive cells at that point. This is referred to as the optic disk. And you may not realize you actually have a blind spot in your field of vision because your brain is very good at filling in that spot. Your brain kind of takes an average of what it's detecting here and here and says, OK, it's probably the same at this point. So it's a blind spot that you don't know you have. There's one other point on the retina that I want to make note of and that is the macula lutea, and in the very center of the macula you have the fovea centralis. This area of your eye-- this area of your retina is the region of sharpest focus, and your vision becomes more fuzzy the further away you get from the fovea. This is why you move your eye in order to look closely at something, because when you are focusing in on something and you want to look very closely at it, you want to take that light that's reflected off that object and send it straight to the fovea centralis where you have the most precise, sharpest view of it. And you can try it right now, take a look at something in front of you and try and see what's in your peripheral vision without moving your eyes. You can see that your peripheral vision is actually quite fuzzy, and that's because objects in your peripheral vision-- the light that's reflecting off them-- is going to regions of the retina other than the fovea centralis. You may have heard of the disorder macular degeneration. Macular degeneration is a loss of vision in the center of your visual field. So you lose vision at the macula and the fovea centralis. And there's two types of macular degeneration, there's what's called wet macular degeneration that's caused by leaky blood vessels under the retina, and then there's dry macular degeneration, which is more common, but we don't exactly know what causes it, and it tends to hit people over the age of 65. Let's talk about the lens of the eye. The lens acts like the lens in a magnifying glass or the lens in your microscope. What it does is it focuses light on the retina. So light that's reflected off of an object in front of you passes through the cornea, through the pupil. And in a lens, the lens controls the pathway of that light-- it bends the pathway of that light so that it's as focused as possible, it's as sharp and precise as possible on the retina. And the ciliary muscles in the ciliary body, as we mentioned, they change the shape of the lens to accommodate either distant or close-up vision. If you remember on your microscope, when you take the letter E on a slide, when you put that under the microscope, what you actually see is that. The image that you see of the letter E is flipped upside down and backwards. Now this actually happens to objects you see out there in front of you as well. So take a look at your computer or whatever you're watching this video on and imagine that the image that is actually hitting your retina is upside down and flipped backwards. Your brain actually straightens this out. So your brain knows that your lens does this and your brain takes that image, and as part of the processing of that visual information, flips it back to right side up in the correct orientation. The lens can become clouded, this is a condition known as having cataracts. It's usually due to an inadequate nutrient supply, and it can be fixed surgically by replacing the lens with an artificial lens. Now the lens is supposed to focus light so that it is most precise on the retina, but sometimes there's a bit of a mismatch between the length of the eyeball and the focal length of the lens. So I want to introduce a few terms here. Emmetropia is the technical term for normal vision, 20/20 vision. You see at 20 feet what normally-sighted individuals see at 20 feet. And this is when you do have a match between eyeball length and the focal length of the lens. So light rays are focused precisely on the retina. Myopia is near-sightedness, and this happens when the eyeball is basically too long. So we can look over here, you've got light coming in, it's bent at the lens, but the point where the light is focused is anterior to the retina. So by the time that light reaches the retina, it kind of extends out, it's all fuzzy again, it's not precisely focused. Hyperopia is the opposite problem. Hyperopia is farsightedness, where the eyeball is shorter than the length of the lens. So when the light actually hits the retina, it's not fully focused yet, it's still a little bit fuzzy. These conditions can be fixed, as we're all probably aware of, by putting an artificial lens in front of the normal lens in your eye. With myopia, you put a concave lens in place and that corrects the focal length to match the retina. With hyperopia, you put a convex lens in place to bring the focal length to match the eyeball. In layman's terms, these lenses are known as either glasses or contacts. Many people also develop presbyopia, and presbyopia is an age-associated hardening of the lens. So normally, remember, that the ciliary muscles allow for the lens to change shape as you focus in on objects close up. But if the lens hardens, it can't change shape in order to accommodate this close-in focusing, so you can't focus as well on objects that are close to you, and many people develop a need to wear reading glasses to correct this. We've touched on the accommodation reflex a few times, let's actually take a look at it now in closer detail. The accommodation reflex is an adjustment of the eye to focus on objects at varying distances. And it involves cooperation between both the pupil and the lens-- both of these adjust to focus on objects that are close. So when you are focusing on something that's close up, the ciliary muscles contract, which actually shortens the lens so the lens is a little bit more rounded. The pupils also constrict to let less light in so you don't have fuzzy edges. But when you focus on something far away, the ciliary muscles relax, the lens flattens out, and the pupils open up a bit, allowing more light through. We've talked about the layers of the wall of the eyeball-- the fibrous' layer, the uvea, the retina-- and we talked about the lens, but we haven't really talked about what fills the eyeball. There are two fluids in the eyeball that are referred to as the humors of the eye. Humors is an antiquated term for the fluids of the body-- basically the Greeks used to think that the body consisted of four different fluids, and that it was a balance between these fluids that made you sick or made you unhappy and that determined your personality even. We know now that the body is a lot more complicated than that, that it can't be entirely described by balances between these four humors, but the terminology still survives in a few different places. One of those places where it survives is in naming the fluids of the eye. So there's two. You have the aqueous humor and you have the vitreous humor. The aqueous humor is in the anterior chamber, the chamber between the cornea and the lens. The aqueous humor is fluid. It's continually renewed and it exists to provide nutrients to the lens and the cornea. You don't have vasculature in your cornea for obvious reasons, it would look quite strange if you were viewing the world through blood vessels. But blood vessels in the chorold release nutrients into the aqueous humor, and those nutrients and oxygen keep the lens and the cornea healthy. The posterior chamber behind the lens is filled with vitreous humor. This vitreous humor is more gelatinous, it's gel-like, it's not fluid. And it provides structural support to the eye, so a counterpressure to keep the eye rounded. The vitreous humor does not-- cannot be replenished. It forms once in the embryo. So if your eyeball gets damaged and you lose the vitreous humor, you lose that structural support, you're basically not going to be seeing out of that eye. Now some of you may have heard of the condition glaucoma. Glaucoma is elevated intraocular pressure. So glaucoma occurs when you have an increase in pressure in the aqueous humor, and that increased pressure in the eye can end up damaging the optic nerve leading to blindness if it's not treated and corrected. Glaucoma really needs to be managed carefully. Now that we've talked about all the terminology, I just want to run over briefly the pathway of light through the eye. So light comes in through the cornea, passes through the aqueous humor, through the pupil and the lens where it gets bent and focused, passes through the vitreous humor before hitting the retina. OK. I do want to talk a little bit about the anatomy of the retina and the different cell types that you find there. So there are two types of photoreceptors that you find in the retina. You have the rods and you have the cones. The rods are effective in dim light and give you peripheral vision. They're more light-sensitive, which is why they allow you to see in dim light, but they aren't as sharp at detection and they actually have no sensitivity to color. So rods are primarily responsible for your peripheral vision, I'd encourage you to grab something brightly-colored and move it out of your visual field. At some point towards your visual field, you will not be able to really see the color. The cones are useful for bright light and for color vision. So you have different types of cones that allow you to detect different colors. They also allow for sharply-focused vision. So cones are highly concentrated in the fovea centralis, that's why the fovea centralis is where you have the sharpest focus, because there is a large concentration of cones at that point. This separation of function between rods and cones, this is also why we can't see color very well in dim light. I encourage you the next time, it's dark out, step outside and see how well you can actually discriminate the colors. Not nearly as well in the dark as you can when you have a brightly-lit area. If you look at the orientation of the retina, it's actually a bit backwards. The photoreceptors, they're the light-detecting cells, you'd expect them to be closest to the vitreous humor, to grab onto that light as soon as it hits the retina. But actually, the photoreceptors are located at the most posterior part of the retina, right up against the pigmented layer. In between the vitreous humor and the photoreceptors, you have bipolar cells and you have ganglion cells. And remember that it's the axons of the ganglion cells that form the optic nerve. This diagram shows those axons collecting together. There is a signaling relay between the photoreceptors, the bipolar cells, and the ganglion cells before the signal is ultimately sent up the optic nerve to the brain. So light comes through this way before being detected by the rods and cones, but then the signaling pathway actually passes that way. As far as what actually happens when your eye detects light, it all involves a complex called rhodopsin. Rhodopsin has two components to it. There is an organic molecule called retinal and a protein component called opsin. Together, retinal and opsin make rhodopsin. Retinal is actually derived from vitamin A, which is why your mother always told you to eat your carrots because it'd be good for your eyes. Carrots contain a lot of vitamin A-- lots of orange vegetables do-- and vitamin A is needed to make retinal. In the dark, rhodopsin accumulates. But when light hits the retina, the energy from the light causes the opsin in the retinal to separate, so the rhodopsin breaks apart. This is an effect called bleaching. This bleaching effect is part of why bright light is blinding, because if you have a lot of it coming in, you have a lot of rhodopsin breakdown, it takes your eyes a few moments to build more so that you can detect the next light coming in. In the light-detecting cells-- both rods and cones, actually-- you have cation channels, sodium and calcium channels that are open in the dark when rhodopsin is accumulating. But when rhodopsin breaks down in the presence of light, these cation channels close. So light causes the cation channels to actually close. What this means is that the detection of light is actually the opposite of what you might think. Rods are actually depolarized in the dark because they have these cation channels opening. So in the dark, rods are sending this continuous signal. They repolarize in the light. The cation channels close, you don't have positive ions moving inward anymore, the rod cells return to resting membrane potential. So it's the absence of the signal, the absence of depolarization that occurs with light detection. But as this absence of depolarization is relayed through the bipolar cells and the ganglion cells, due to that neurological relay system, you get depolarization sent along the optic nerve in the presence of light. And I, again, refer you to the phototransduction video for a good walkthrough of that process, that relay process. The basic process of the excitation of cones is really similar to the excitation of rods. However, the rhodopsin molecule is a little bit different. It's actually not called rhodopsin in cones, it's just referred to as a visual pigment. But the visual pigment in cones, they have the same retinal, but the opsin varies a bit, it's a little bit different. And this difference in the opsin protein means that cones are a lot less sensitive [than] rods, so they can be excited only by bright light. It also means that cones respond to different types of color, different wavelengths of color. There's actually three types of cones. There are cones that respond to a blue wavelength of light, cones that respond to a green wavelength of bright light, and cones that respond to red. So the information that your brain is actually getting is percentages of blue cones activated and green cones activated and red cones activated. If you had, for example, a light hitting a patch of cones on your eyes and stimulating 100% of the blue cones but not stimulating any of the green or red cones, you'd see a very pure blue color. If you have light hitting an area of your macula that stimulates blue and red cones but doesn't stimulate any green cones, your brain would interpret that information as purple. So it's stimulating multiple types of cones and variations in the strength of stimulation of each type that gives us the wide spectrum of color vision that most people have. However, there are people that have a genetic lack of either red cones or green cones. This is where color blindness comes from. All right, there's a lot of information in this video. After studying it, you should be able to talk about the anatomy of the eye, explain the accommodation reflex, how changes in the pupil and lens work together. Talk a little bit about how that happens, so both how the pupil changes size and how the lens changes shape. You should be able to explain cataracts and myopia, and actually we mentioned macular degeneration as well. You should be able to distinguish between rods and cones and describe the role of rhodopsin in activating rods.