Term
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Definition
Light goes through different media:
Besides geometrical constraints, the media have particular optical properties
Here you have a schematic, a very simple schematic of the main parts of the eye. And you have, for instance, the lens, and then you have in here at the very beginning, you have aqueous humor in this compartment. And then you have the lens, and then you have another compartment filled with vitreous humor. And in the back of the retina is that finally you have photoreceptors.
The point I want to make with this diagram is that light has to travel through different media. If you ever put a pencil inside of a glass full of water, you know what happens to the visual spectrum when light changes medium. Everything is changing. So going through the different medium, everything is going to be changed. There are geometrical constraints, of course. And the media is having different optical properties. |
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Definition
Images in the Retina Are Reversed and Inverted
Concepts:
• Orientation: nasal, temporal
• Macula: central vision, ~1.5 mm Fovea: highest acuity
• Blind spot: about 15o medial (on the retina) to the fovea
Fovea: Region of highest visual acuity Central 1–2o of visual space Takes about 1/2 the fibers of the optic nerve
In particular, I want to point out a couple of them. Images in the retina are both inverse and inverted. Now, what I mean by the first one is that, for instance, if you have an arrow pointing to the right, actually, the way it is depicted in the retina, it will be pointing to the left. So everything has been reversed. |
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Term
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Definition
Images in the Retina Are Reversed and Inverted
Notice:
• Upper visual space projects onto lower retina
• Lower visual space projects onto upper retina
The other concept-- that being inverted refers to the up and down direction. So if now the arrow is pointing up, the way it is projected into the retina is going down. Remember, this is happening because of the different optical properties that are in the different media that the light is traveling. The light brings information, and that information is starting to be distorted, if you would, because of the optical properties of this system involved.
The upper visual space projects into the lower retina, and the lower visual space projects into the upper retina. These things are important to understand, because it will make sense later for you to be able to follow the path of the light when trying to determine different deficits. Now, there are several things that you need to keep in mind. The retina is the retina. And the space in the retina is the space in the retina. When we talk about the visual field, we are talking about the field out there, the stuff that you see in the environment. So that's your visual space.
When you don't see something, because there is a problem in the retina, yes, the problem might be in the retina, but what you don't see is in the field, in the visual field. The lower part of the field, remember, is going to the upper part of the retina. The upper part of the visual field is going to the lower part of the retina. The left to the right, and the right to the left. Because after all, it's going into a cup like that. So light is travelling from the bottom to the top, from the top to the bottom, left and right, and so on.
So if you have a problem in the upper part of the retina, what you may not see in the field is something which is in the lower part of the visual field. Keep that in mind, because that will help you understand deficits in the visual field. |
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Term
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Definition
Light has to travel through the cellular layers in order to hit the receptors in the back of the retina. The fovea is the place of highest visual acuity.
Now, importantly also, some of the details here. We have the photoreceptors are the last layer of cells in the retina. So it's a very interesting system. The light has to travel through different cellular layers before it actually hits the photoreceptors, the ones which are actually going to react to the light. Light at the fovea-- again, this place in here. The fovea is the place of the highest visual acuity. In terms of the photoreceptors, we have rods and cones.
Cones, with C, it's for color vision. With cones, you have color vision, and you have a larger concentration of cones very close to the fovea, the fovea place. Night vision, we see with the rods. Rods don't give you color, but we have a lot of rods also in the periphery. So when under very little light, we are still able to see, and we are using our rods. This is why you don't see color when it's dark, but you might still see movement, and you may still see things that are there in the visual field |
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Definition
Light is transformed to electrical signals by photoreceptors and the signal transferred from photoreceptors to ganglion cells by specialized interneurons
In this diagram, you have the names of the different cellular layers and some of the details of the cells themselves. You have bipolar cells, and ganglion cells, and horizontal cells, and some other types. Now, in here, you have actual histology, showing you, again, the different types of layers in the retina. Light, again, is travelling through all of these guys before it hits the rods and cones, which are in the back of the retina. And then light is transformed to electrical signals by these photoreceptors.
Here you have the ganglion cell layers. These I'm going to show you next. They are important cells, the only ones in this area that are able to fire action potentials. So let me show you a little bit of the circuitry in the retina. |
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Term
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Definition
• Dark: Na+ keeps going into
the cell
• Light: closes Na+ channels and hyperpolarizes the receptors
RGC are the only cells in this circuit that fire APs
• P ganglion cells: smaller fields, more numerous, respond to color and are used in the perception of fine detail; project to the parvocellular portion of LGN
• M ganglion cells: large receptive fields, respond best to large objects in the visual field and are responsible for the perception of movement and rough analysis of shapes and forms; project to the magnocellular portion of LGN
• K ganglion cells: project to all layers of LGN
Here you have the circuitry. On the right-hand side, you have the photoreceptors. Remember, these photoreceptors are at the back of the retina. So light is basically going this way. It's going up in your screen, and it's bypassing the ganglion cells and their axons. And then the amacrine, and the bipolar, and the horizontal cells. This, of course, is an easy way to understand the circuit.
And it is true-- It's a true circuit. But it's heavily simplified. It's much more complex than this, but this still conveys the main idea. The photoreceptors are going to be communicating information to the bipolar cells. And the bipolar cells will then send information to the ganglion cells.
Now, I already told you, the only cells firing action potentials in here are the ganglion cells. In between, you will notice already horizontal cells and amacrine cells. These are able to affect the communication between photoreceptors and bipolar cells.
Now, I tell you right now, if we thought of potassium as the main ion involved in the vestibular and the auditory systems, sodium is the one that is going to be important here. And we are going to be talking about a dark current. This is because sodium is always leaking into these cells. Light closes sodium channels and hyper-polarizes the receptors.
So sodium, which is a positive ion, is keeping them depolarized. When light comes in, it closes them, and then they hyper-polarize. It's a very interesting system, because it sort of works backwards from what we have been discussing in terms of other systems. Retinal ganglion cells, again, are the only cells in this circuit that fire action potentials.
Now, there are different flavors for all of these different types of cells. For ganglion cells, there are different descriptions, and there are P, and M, and K, and so on. We don't have to get into all of that detail, but it's important for you to be aware of differences at the cellular level. |
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Term
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Definition
Center—Surround Receptive Fields
-Bipolar: ON cells respond to presence of light and therefore are hyperpolarized by the sustained release of neurotransmitter by photoreceptors in the absence of light. OFF cells respond to the absence of light.
ON- and OFF-center RGC
•Center—Surround Receptive Fields
RGC: ON center responds to the presence of light with depolarization when the light is on the photoreceptors at the center of the retinal receptive field. RGCs respond best to differences in illumination.
ON- and OFF-center RGC
I want to move now into a concept that is sometimes a little bit difficult to understand. It centers around receptive fields. Now, let's put this aside for one second and remember basic things. When we talk about pain and temperature or pinching in our fingers or things like that, we were always talking about a receptive field. The concept of receptive field is the area from which we are able to recover information, the area from where we get information.
In the case of the visual system, the visual field is the area in a space where we are receiving that information. In terms of the circuitry that is involved, we have then the concept of surround receptive field-- center and surround. And it is depicted in here. Simply, we can keep it as simple as possible. On center, ganglion cells. Now, in reference to those particular cells, you can see if the light in here is at the center of the field-- the cell is able to fire. And so it's carrying that information that is at center. It's tuned to detect the light that comes in the center.
If, on the other hand-- and it's not firing to the darkness on the sides. If you put the light here on this side, then you can see that it's not firing that much. These little ticks in there represent action potentials. So this is the stimulus. Now, if what you have is an off-center ganglion cell, that means that it responds heavily-- it's going to fire heavily when the light is off center, when it's on the periphery. OK?
So it's the combination. Unfortunately, again, we don't have time to get into a humongous amount of details. But put this together-- what I was telling you about the organization of the circuit. And now you will understand that information is being conveyed from the center and also from the periphery in the visual field. And this information somehow is making it into the bipolar cells and from the bipolar cells into the corresponding ganglion cells. And these ganglion cells are now able to fire action potentials and inform the visual cortex as to what is happening, inform the brain, the rest of the brain as to what is happening for interpretation of the signals.
Now, it's the combination, a very large combination of these types of circuits, that allowed us to see all types of situations. We are particularly good at seeing borders, or determining changes in contrast. We may not be as good as other species in terms of detecting small details or anything like that. But our visual system is good enough for us to survive. |
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Term
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Definition
Rods contain more photopigment (opsins)
Rod are more sensitive to light (respond to one photon) Cones need 10–100s photons to activate
Next, I'm going to show you some of the concepts that have to do with the photoreceptor and the spectra that we are able to see. So remember, in the auditory system, I said we are able to hear between 20 hertz and 20 kilohertz. Following the same logic, in here, we are able to see between about the higher 300s, around 400 nanometers-- this is for the wavelength-- close to the 700 nanometer. This is our visual spectrum.
Now, of course, you have a higher area where you have mostly blue, and mostly green, and then mostly red, and so on. And we have the same flavors for our cones. So our cones, there is a set of cons called blue cones, basically, that are very good at detecting this type of light, light at around 430-something nanometers. And then green cones, which are detecting very, very effectively light that comes at around 530-something nanometers. And then red cones.
So basically, we have a system that consists of blue, green, and red. And together, with those among them and a little bit of different flavors here or there in terms of what they are, these are S, and M, and L type of cells. The combination of all those colors is what allow us to take an infinite, basically infinite, amount of colors in the spectrum.
On the other hand, the rods, which contain more photo pigment options, are able to respond even to one photon, are unable to move. You only have about one base spectrum very close to 500 nanometers. Now, if you read different textbooks and so on, there will be small differences, and this is why I put this other spectrum in here. Small differences in what people will report. So don't be concerned with little things like that. If the blue cones are here able to be based at around 437 nanometers, this is according to these investigators. And then some other investigators may have found, using similar or different techniques, 440 nanometers. So a couple of nanometers here or there or something-- nanometers or something is not really going to make such a big difference. The important thing is to remember the concept. |
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Term
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Definition
Light closes Na+ channels
Now, when we move in to seeing photo transduction, this is what I described before when I was telling you sodium is all the time common into the photoreceptor. So we call it the dark current, and it's, again, sodium-mediated. When light comes in, everything changes. The sodium channels are closed. And then this receptor is going to hyper-polarize. Here you have an example of that from the electrophysiological point of view. You have a light flash, and then you have hyper-polarization of the receptor |
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Term
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Definition
Molecular steps in photo-transduction:
Light enters the eye and hits the G-protein coupled receptor: opsin (e.g., rhodopsin). Photon absorption causes 11-Cis-retinal to undergo isomerization to all-trans which causes a conformational change in the rhodopsin (this activated form is called metarhodopsin II). Activated rhodopsin causes reduction of intracellular concentration of cGMP. How? The intracellular concentration of cGMP is controlled by a phosphodiesterase (PDE) via another G-protein called transducin. cGMP is what keeps Na+ open; the PDE hydrolyzes cGMP into GMP. Lower concentration of cGMP closes the Na+ channels, so the cell hyperpolarizes.
One concept that I want you to get familiar with that sometimes confuses students is the change in the shape of the protein. For instance, this, the photon absorption here tells you it's changing 11-Cis-retinal, going isomerization to all-trans. It's a conformational change. And sometimes people don't understand what it means, "conformational change." It's nothing else that imagine this is the protein. My hand is now into this confirmation. And something happens to it, and it changes conformation. It changes shape. In this case, it's a changing shape.
So because of these changes, it will also change its function, or its ability to perform a particular task. Now, this cascade of events eventually will result in-- follow their steps up to here, and you will see that it will result in the isomerization of this PDE, the esterase, and hydrolyzes to cyclic [INAUDIBLE] monophosphate. And therefore, all of these concentrations change. And that's how, eventually, phototransduction is going to take place. When the cell hyper-polarizes, remember, at the end of all of these events, calcium has to come in to be able for neurotransmitter release to happen. |
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Term
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Definition
Visual Pathways From Retina to Visual Cortex
SC: reflex movement of eyes and head; the tracking of visual stimuli
Suprachiasmatic nucleus:
neuroendocrine regulation
Pretectal areas: pupillary light reflex
So here you have, again, a schematic of the main pathways from the optic nerve going to the lateral geniculate-- remember lateral geniculate nucleus is part of the thalamus-- and then from there to the primary visual cortex. About 10% of the axons actually bypass the lateral geniculate and go straight into the superior colliculus. From there they project to the pulvinar, also one of the nucleus of the thalamus, and then to the cortex.
These are extrageniculate pathways. You saw this before. I hope you remember with one more detailing here going to the pretest and that's when we did the pupillary light reflex. Now I have removed some of the information and put some other important information.
So out of about 1,200,000 axons in the optic nerve per eye, about a small percentage of those will bypass also the lateral geniculate but are not going to go through the superior colliculus. They might go to through the suprachiasmatic nucleus of the hypothalamus, again, to pretectal areas. So we call all of these guys extrageniculate pathways. |
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Term
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Definition
The LGN is a six-layered structure
Inputs from the ipsilateral eye are projected to layers 2, 3, 5.
Inputs from the contralateral eye are projected to layers 1, 4, and 6. Hence: there is no binocular
fusion = segregation
Layers one and two consist of larger neurons:
Magnocellular: movement and contrast
Layers 3–6: smaller neurons
Parvocellular: color and form
All six layers also receive input from the non-P non-M type konicellular retinal ganglion cells.
Now when we put a dye in the retina and we are able to follow the pathways of the axons and so on, you will realize that everything is segregated. All the inputs are segregated. This is a view, a couple of views of the lateral geniculate nucleus of the thalamus, the visual thalamus. And what you have here is that input. The lateral geniculate has six layers. The six layers are segregated. The inputs coming from the ipsilateral eye are coming into layers 2, 3, and 5. And from the contralateral into two layers 1, 4, and 6.
Now to some extent this should not be surprised, because, remember, the light coming into the eye is then following to a couple of different pathways. One which is ipsilateral and the other one, which is contralateral. And those axons are crossing of the optic chiasm.
When we go into look into the details of the lateral geniculate, what you'll see is that there are two main types of cells and there are two main types layers, magnocellular and parvocellular. Magnocellular, as the name indicates, magno is big. So these are big cells. And these cells are very, very effective at detecting movement and contrast. On the other hand, parvocellular layers are very good at detecting color and form. |
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Term
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Definition
Visual Thalamus: LGN
Let me show you another little detail here. This is another way to look at that. What you have in terms of going from one to six is that they have, again, organization. Now layer one is receiving from the contralateral and layer two from the ipsilateral. And they go contralateral, ipsilateral and then ipsilateral, contra, ipsi, contra. So these are parvocellular layers and these are magnocellular layers, that is in terms of the organization of the lateral geniculate. |
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Term
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Definition
Geniculocalcarine Pathway: Optic Radiation
Cortex is also a six-layer structure:
Inputs from the LGN come mostly to layer 4 (4c): 4Cα for magnocellular input
4Cβ for parvocellular input
When we go from there, the information from the lateral geniculate is going to be sent to the primary visual cortex. Remember that is around the calcarine sulcus, area 17, in the occipital cortex in the back of the head. And there it will look something like this. This is actually histology in that area. And there are so many cells in layer 4, granule cells in layer 4, and so many axons going out with information that they form something called the stiria of Gennari that is visible here.
You don't need a microscope when looking at a section through the visual cortex to be able to determine the border between area 17, primary visual, and area 18 which is non-primary, but is still higher visual cortex. And here you have the picture on the diagram of the input from the lateral geniculate into layer 4C of the cortex.
Layer 4, again, is so large that it's divided usually into alpha, beta, and gamma; or 1, 2, and 3; or A, B, C, but at least three different components. It depends on which text you are reading or how much research is being done in a particular area. |
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Term
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Definition
Striate Cortex (Primary Visual Cortex)
Now when-- it's amazing, at least it's amazing to me, that all of the inputs are still being segregated. And this is what is being shown here with cytochrome oxidase blobs. And then in here, again, showing ocular dominance columns, the segregation of pathways.
A couple of very famous people that work heavily in the visual system were Hubel and Wiesel who talked a lot about ocular dominance columns. Ocular dominance is in reference to the fact that one eye is dominant for one particular column and then the other eye is dominant for the next column. And this is how those columns may look like. If you go back to some of the representation from the optics, you have something very similar in there that I use to illustrate the concept of columns. |
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Definition
Visual Pathways and Retinotopic Organization of the Visual Fields
Inferior fibers: Meyer’s loop passes through the temporal lobe
Superior fibers: pass through the parietal lobe
Lower visual field goes to the superior retinal quadrants; fibers from the superior retinal quadrants project to the medial half of LGN
Upper visual field goes to the lower retinal quadrants; fibers from the inferior retinal quadrants project to the lateral half of the LGN
In the visual pathways when we look at the visual pathways and follow the pathways, we're find that it is retinotopic. So remember in the auditory topics, we talk about tonotopic. So there is a map with the different frequencies. Here we talk about retinotopic. There is a map of the visual field.
There are a couple of important pathways to remember, and I will show you this in a second, pathways that go into something called Meyer's loop, and then some that go on top which are different. In here what I went to illustrate, these are inferior and superior fibers, by the way, inferior, again, layer and superior that pass in through the parietal lobe.
But the more important, the most important point that I want you to notice here is that in color, you have color coded images here. So if you just take this eye and you look at the colors, you will realize that you have a disproportionate amount of a cortical area devoted to the most central part of the visual field, to the fovea, basically. And then as you move away from there, the visual field gets bigger but there is less cortical area devoted to those fields.
You will also notice that the upper part of the field of the visual field in these colors here ended up in the lower bank of the calcarine sulcus and then that the lower part of the visual field ended up in the upper.
Now this thing, the fact that you have so much in real estate, so much brain devoted to the central part is one of the reasons why you have macular sparing. The concept is that if you were to have a deficit that is central, you might still be able to see very well because you have so much in the brain devoted to pay attention.
This is also the reason why although we use our eyes for a very particular spot in the visual field, there's this part to which we are paying visual attention. Now we are still collecting visual information from the periphery. But if something was to pass by here, I might detect that something moved, but I will not be able to tell you any of the main details of what it was that moved. |
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Term
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Definition
Dorsal and Ventral Streams of Higher Order Visual Processing
Another important concept that I want you to remember is the concept of the dorsal vessels, the ventral streams. This is for higher order visual processing. And the idea is that the dorsal stream is in charge of where and the ventral stream is in charge of what. So here you have analysis of motion in relations in a space, while here you have analyzes of form and color.
Underneath here you are unable to see. You have the fusiform gyrus, which is both in the recognition of faces. Th deficit that results from damage to that is prosopagnosia, you are unable to recognize familiar faces. You can get other deficits, we'll talk a little bit more about that in clinical correlations, such as achromatopsia, and so on, inability to see colors. |
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Term
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Definition
Dorsal and Ventral Streams of Higher Order Visual Processing
Going back to this dorsal and ventral streams, I just want to point out with this that things always get much more complicated. And then you have M cells. You have P cells and so on, getting into very particular areas of layers. For instance here, layer 4C alpha, while this is going to 4C beta and so on.
There is no need to get into this amount of detail. But suffice it to explain to you for you to keep in mind, you have the dorsal stream, the ventral stream. And they seem to exert to a great extent very particular characteristics of the visual field. Some are better for understanding color and form and shape than what. And some are better for understanding what is moving and where it is going and the direction of movement and things like that. |
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Term
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Definition
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Term
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Definition
| farsightedness and results from an eyeball that is too short (image converges behind the retina) |
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Term
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Definition
| is near sightedness and results from an eyeball that is too elongated (image converges in front of retina) |
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Term
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Definition
| condition in which the eye exhibits a progressively diminished ability to focus on near objects (usually as a result of aging) |
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Term
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Definition
| (Greek for darkness; plural: "scotomas" or "scotomata”) an area of partial blindness surrounded by a field of normal—or relatively normal—vision |
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Term
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Definition
| (or hemianopsia; hemi = half) a half visual field that is lost with respect to the vertical midline; usually affects both eyes, but can involve one eye only; homonymous hemianopsia occurs when there is hemianopic visual field loss on the same side of both eyes |
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Term
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Definition
| same as before, but for a quadrant of the visual field (1/4) |
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Term
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Definition
| any or all of a set of medical conditions in which the individual is unable to perceive color (either fully or partially) |
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Term
| There are two major families of non-homologous opsin proteins: |
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Definition
• Type I—used by prokaryotes
• Type II—used by animals |
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Term
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Definition
| a group of light sensitive membrane bound G protein coupled receptors |
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Term
| Five groups of opsins are involved in vision |
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Definition
| (there are other opsins, but they are not involved in vision, e.g., melanopsin—circadian rhythms) |
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Term
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Definition
| used in the context of cortical lesions—the fovea has a relatively large representation for its size (notice seven slides back that the number “1” is small in the visual field, but occupies a relatively large area of the cortex... a lot of cones code for the central vision!); so... some of the areas can be spared |
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Term
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Definition
Visual Deficits Due
to Lesions in the Pathways
More importantly, I think we can devote a little bit of time in trying to understand these different deficits. And here I would like you to be able to practice on your own, to go through this slide, and then test yourselves to be able to determine the deficits that might result. So we are only going to do a couple of them, and then you should practice on your own. Make sure that you understand why it is that you don't see in the visual field whatever it is that is not being seen.
So in this case, it's very easy because what you have lost is a complete eye-- the right eye. So when you have something like that, it's a monocular visual loss of the right eye. This is B. So of course, if you make a cut here of the whole optic nerve coming from that eye, then you don't see anything with that eye. And everything in that visual field is gone.
If you have a scotoma-- as you have in A-- pay attention to the visual field. The scotoma is on the right eye and is on the left side of the visual field of the right eye. So that is because the actual damage in the retina is on the opposite side to where you have it in the visual field. Remember, that is because the light coming from this side of the visual field-- so that's the side of the visual field-- is not being collected at the side of the scotoma.
Now, if you follow-- so there is a way to understand and do this exercise-- is follow the pathway of the light. That being said, you can get bitemporal problems-- bi- because it's both, temporal because-- remember I said, nasal versus temporal? So this is towards the temples. You can have contralateral superior quadrantanopias-- superior because they are in the upper part of the field, quadrantanopias because it's only one quadrant.
So just make sure to be able to follow the pathway of the light and then to arrive at the different deficits. Be also aware that you may get similar deficits with lesions which are in different parts of the field. Just do this exercise. You should be able to do it on your own. And it's important to do it and understand the pathway of the light. |
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Term
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Definition
Now, this is a view of a human brain, now with some areas that have been removed to show you optic radiations and to make a few important points. These are fibers now coming from the thalamus into the primary visual cortex. So you can follow it this way. And it's going into areas around the calcarine sulcus. So remember, this is area 17-- primary visual cortex.
Now, one point is that this is nice as an illustration, but one important point that I want to make is for you to be aware of the following. You have the eyes here, in the front of the brain. And so visual information is being collected and is being sent all the way-- the different stations-- but all of the way to the back of the brain. That makes the visual system extremely useful in terms of diagnosis.
There are many things that can happen that will influence the visual system that are not really related to the visual system. For instance, a tumor that might be growing at this level might be pushing into the optic chiasm, and therefore, the patient may experience visual deficits. And because of those visual [? deficits-- ?] the visual deficits are easy to diagnose because the patient is usually able to tell the doctor what it is that is bothering them.
Or they can be tested and the doctor can determine what it is that the patient is unable to see, and then, it's very useful for diagnosis. The different places also, because all of the inputs are being segregated, remember? That may also help in the diagnosis. So the visual system is important for diagnosis. Because it's interesting that it's able-- it has to travel all the way from the front to the back. So it's particularly good to detect any problems along the way. |
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Term
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Definition
Do Not Believe Everything You See... the Visual System Is Easy to Fool!
Now, finally, I want to make the following point. What you have here is an illusion. I think most of you-- about 99% of the people-- will think that there is something that is moving. I can prove absolutely, without any doubts, that there is nothing here that is moving. Your system has been fooled. The reason we are able to do this is because of the geometry and the color. And so some of the cells are fooled into detecting movement when there is nothing moving.
Now, this is interesting for fun, but this is also important. It has legal implications. This is, for instance, what happens in a court of law when a lawyer is questioning a witness and they say, so how far away were you from the events that you described? And how dark was it? What time of the day was it? And then they will tell you, well, you are simply-- you were unable to see what you claimed that you saw because it's not possible for the visual system to function that way because it was dark. You could not possibly see color in the dark-- and things like that.
So the visual system is easy to fool. This is also great for magicians. And this is how magicians work. They fool our visual systems very effectively |
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Term
| A contralateral superior quadrantanopia can result from damage to what? |
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Definition
| Damage to Meyer’s loop on either side |
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