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What is the direction of the processing of light by the (human) retina and how does it happen?

What is the direction of the processing of light by the (human) retina and how does it happen?


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Quoting Textbook of Medical Physiology by Guyton and Hall, 2016, page 647,

… the functional components of the retina, which are arranged in layers from the outside to the inside as follows:

(1) pigmented layer, (2) layer of rods and cones projecting to the pigment, (3) outer nuclear layer containing the cell bodies of the rods and cones, (4) outer plexiform layer, (5) inner nuclear layer, (6) inner plexiform layer, (7) ganglionic layer, (8) layer of optic nerve fibers, and (9) inner limiting membrane.

After light passes through the lens system of the eye and then through the vitreous humor, it enters the retina from the inside of the eye (see Figure 51-1); that is, it passes first through the ganglion cells and then through the plexiform and nuclear layers before it finally reaches the layer of rods and cones located all the way on the outer edge of the retina. This distance is a thickness of several hundred micrometers; visual acuity is decreased by this passage through such nonhomogeneous tissue. However, in the central foveal region of the retina, as discussed subsequently, the inside layers are pulled aside to decrease this loss of acuity.

I have attached Figure 51-1 for people who would like to see it.

My questions are: How does light travel to the inner parts of the retina first even when there are so many impeding layers preceding it? Why does it not stimulate the photoreceptors first? What is the pathway of the light after it travels to the the innermost retinal layer? Are the photoreceptors the first to be stimulated by the light?

As can be understood, I am quite confused, so if the framing of any question is reflective of erroneous understanding, kindly let me know. All help appreciated.


Short answer

Photoreceptors are the only cells in the retina that directly detect light; they can detect light through the other layers because those layers are so thin and effectively transparent: light passes right through to the photoreceptors.

Longer answer

The retina is fairly thin, and the bipolar/RGC layers don't contain much pigment. Have you ever looked at a thin slice of tissue under a microscope? You can do this and focus to different layers because single layers of cells are fairly translucent (remember they contain a lot of water): most light passes right through them. Some cells, such as red blood cells or photosynthetic plant cells, are harder to see through, but that's only because they are full of pigments.

The reason the photoreceptors respond to light in a way that can be detected biologically is that they contain special photosensitive pigments. In rods, this pigment is called rhodopsin and it is composed of a protein and a molecule of retinal. Most other cells in the retina don't have any such photoreceptors (there is a special class of retinal ganglion cells that is an exception, see for example here - these cells have a pigment melanopsin and contribute to light detection for circadian rhythms rather than vision).

Other cells in the retina respond to light only because they are sensitive to neurotransmitters released by photoreceptor cells and other retinal cells.

As far as why this is the arrangement, with photoreceptors in the back, it's really just a fluke of evolution and evidence that evolution and not design is the best explanation for diversity in biology. Eyes have evolved more than once in animals, however, and cephalopods like squid do not have their retinas arranged this way; in squid the photoreceptors are the most superficial layer.

Because the retina is so thin, this arrangement doesn't provide a large enough disadvantage to be selected against given the complexity in changing the organization. One exception to the thinness, however, is in the blind spot. The blind spot exists because all of the axons from the retinal ganglion cells have to exit the retina someplace. They exit in a big bundle, and there can't be any photoreceptors where that bundle is, so there is a spot where you cannot see. However, the position of the spot is not in the center of your vision, and that part of the visual field is usually covered by the other eye


  • Sensory signals are converted to electrical signals via depolarization of sensory neuron membranes upon stimulus of the receptor, which causes opening of gated ion channels that cause the membrane potential to reach its threshold.
  • The receptor potentials are classified as graded potentials the magnitude of these potentials is dependent on the strength of the stimulus.
  • The sensory system shows receptor specificity although stimuli can be combined in processing regions of the brain, a specific receptor will only be activated by its specific stimulus.
  • The brain contains specific processing regions (such as the somatosensory, visual, and auditory regions) that are dedicated to processing the information which has previously passed through the thalamus, the &lsquoclearinghouse and relay station&rsquo for both sensory and motor signals.
  • The four major components of encoding and transmitting sensory information include: the type of stimulus, the stimulus location within the receptive field, the duration, and the intensity of the stimulus.
  • membrane potential: the difference in electrical potential across the enclosing membrane of a cell
  • action potential: a short term change in the electrical potential that travels along a cell
  • transduction: the translation of a sensory signal in the sensory system to an electrical signal in the nervous system

How do contact lenses work?

How contact lenses work to correct vision is the same way eyeglasses do: They alter the direction of light rays to focus light properly onto the retina.

If you are nearsighted, light rays focus too early within your eye — they form a focus point in front of the retina instead of directly on it.਌ontact lensesਊnd਎yeglasses਌orrect nearsightedness by diverging light rays, which reduces the eye&aposs focusing power. This moves the eye&aposs focus point backward, onto the retina where it belongs.

If you areꃺrsighted, your eye does not have adequate focusing power — light rays fail to form a focus point by the time they reach the retina. Contact lenses and glasses correct farsightedness by converging light rays, which increases the eye&aposs focusing power. This moves the eye&aposs focus point forward, onto the retina.

Contact lens and eyeglass lens powers are expressed in਍iopters (D). Lens powers that correct nearsightedness start with a minus sign (–), and lens powers that correct farsightedness start with a plus sign (+).

So why are contact lens so much thinner than eyeglass lenses?

In large part, it&aposs because contact lenses rest directly on the eye, instead of roughly a half-inch (12 millimeters) away from the eye&aposs surface like eyeglass lenses.

Because of their proximity to the eye, the optic zone of contact lenses (the central part of the lenses that contains the corrective power) can be made much smaller than the optic zone of eyeglass lenses.

In fact, the optic zone of eyeglass lenses is the entire lens surface. The optic zone of contact lenses is only a portion of the lens, which is surrounded by peripheral fitting curves that do not affect vision.

It&aposs something like looking out a small window in your house: If you are standing very close to the window, you have a large, unobstructed view of the outdoors. But if you are standing across the room from the window, your view outside is very limited — unless you have a much larger window.

Because contact lenses rest directly on the਌ornea, their optic zone only needs to be roughly the same diameter as the pupil of the eye in low-light conditions (about 9 millimeters). In comparison, to provide an adequate field of view, most eyeglass lenses are greater than 46 mm in diameter. This larger size makes eyeglass lenses much thicker than contact lenses.

Also, eyeglass lenses must be made much thicker than contact lenses to keep them from breaking upon impact. Lenses for nearsightedness in eyeglasses must have a minimum center thickness of 1.0 mm or greater to meet impact resistance guidelines.

Contact lenses can be made much thinner. In fact, most soft contact lenses for nearsightedness have a center thickness that is less than 0.1 mm.

So it&aposs the combination of significant differences in wearing position, optic zone diameter and minimal thickness to ensure structural integrity that makes contact lenses much, much thinner than eyeglass lenses of the same power.


THE CORNEA

The eye is enclosed by a tough white sac, the sclera. The cornea is the transparent window in this white sac which allows the objects you are looking at to be carried in the form of light waves into the interior of the eye.

The surface of the cornea is where light begins its journey into the eye. The cornea’s mission is to gather and focus visual images. Because it is out front, like the windshield of an automobile, it is subject to considerable abuse from the outside world.

The cornea is masterfully engineered so that only the most expensive manmade lenses can match its precision. The smoothness and shape of the cornea, as well as its transparency, is vitally important to the proper functioning of the eye. If either the surface smoothness or the clarity of the cornea suffers, vision will be disrupted.


Questions and Answers

How does the structure of the rod cell help in its function?

How is the way the rod cell built help the cell to do its job? Your article does not tell how the structure of the rod cell helps the cell to do its job.

Here are a few examples of how the structures of the rod and cone cells affect their function: 1) The rod cells have more photopigments, therefore allowing the rods to function better in less intense light and in night vision as compared to the cone cells. 2) The rod cells have highly convergent pathways thus allowing them to have better response in scattered light. 3)The rod cells respond to one single photon thus making them more sensitive. For more details please contact us.

How does the structure of rods and cones adapt to their function?

I need to know how the structure of these specialized cells adapts to their function. The question is on the web but no answer is given so I would like to know because it I quite urgent

The rods or cones have different structures and because of that, they have different functions. For example, the rods have more stacked disks (the disks are the spaces where the photopigments are found). More disks imply more photopigments, and more photopigments mean more sensitivity to light. That is why the rods are more sensitive to light than the cones. The cones have less stacked disks in their outer membrane, therefore much fewer photopigments, and this characteristic makes them less sensitive to light.

Why are photoreceptors in the eye the shape they are?

Why are rod cells rod shaped? Why are cone cells cone shaped? I can't find anything detailing why this is the case, apart from 'it was beneficial from an evolutionary point of view'. But why?

The best way to explain why human photoreceptors are shaped the way they are is by comparing human eyes to the eyes of other mammals. The rods in the human eye differentiate between light and dark while the cones differentiate color. The human eye has about 120 million rods to process light and dark and about 6 million to process color. Humans are trichromatic and able to see three different colors. The reason for the shapes of cones and rods is to enable conversion of light into signals that can trigger responses and allow us to "see." The real evolutionary consideration is the reason for the number and type of photoreceptors in the eyes. The number and shape of photoreceptors have evolved through the evolutionary need of the mammals. For example, owls have much more rods than humans for heightened sight in the dark. Dogs are dichromatic and have additional rods so they can see better in the dark and navigate movement better than humans. These differences make the evolutionary benefits in the different photoreceptors between mammals.

Jamie, what are the three types of specialized cells found in the human eye?

The three types of photoreceptor cells in the eye are rods, cones, and photosensitive retinal ganglion cells. Photosensitive retinal ganglion cells were discovered in 1991, and although they do not directly contribute to sight, they assist circadian rhythms and pupillary reflex.


The Fovea Centralis

Though the eye receives data from a field of about 200 degrees, the acuity over most of that range is poor. To form high resolution images, the light must fall on the fovea, and that limits the acute vision angle to about 15 degrees. In low light, this fovea constitutes a second blind spot since it is exclusively cones which have low light sensitivity. At night, to get most acute vision one must shift the vision slightly to one side, say 4 to 12 degrees so that the light falls on some rods.


The eyes have it

The eye is a wonderfully complex thing, some estimates say up to a third of the average human brain is devoted just to processing the information that comes in. And just like a camera is a collection of complex parts all working in harmony, so is the human eye.

The cornea is at the very front. It’s a curved piece of tissue that serves to protect the rest of the eye, and to help focus the incoming light through your pupil, so you can see things clearly.

Because really that’s what your eye is, a fleshy camera.

Behind the cornea is the iris, the pretty, colouredy bit. The iris is the aperture for your eye. It controls how much light goes in through your pupil. Muscles all around can contract the iris and change the shape of the pupil, contracting if there’s too much light, or widening if there’s not enough so it can take in all the light it can when it’s darker.

Behind the iris is the lens. The lens works with the cornea to focus light onto the back of your eye. Although the lens doesn’t bend light as much as the cornea, it can change shape and focus light differently depending on how far away the object is.
Your lens also cuts down on the amount of ultraviolet light you can see. In his later years the painter Claude Monet had one of his lenses removed, letting in more ultraviolet light, as so his late paintings all have a purple hue to them.

If you’re short-sighted, or myopic, your eye focuses light to a point before it hits the retina. Maybe your eyeball is elongated like a rugby ball, instead of round like a football. So to correct this, you might wear glasses that diverge the light a bit before they reach your cornea.

At the back of the eye you’ll find the retina. I mean, it’s there, don’t go looking, you’ll poke yourself in the eye.

The retina consists of layers of modified neurons, nerve cells, arranged across the back of your eye. Since you can see the retina with a decent camera, it’s the only part of the nervous system that can be visualised directly without having to go inside the subject. Which is nice.

The retina does the job of detecting the light that falls on the back of the eye and turning it into electrical signals the brain can understand, and there are two main types of cell that help with that, rods and cones.
Rods are well…rod shaped, are very sensitive to light and are very densely packed in the eye. In fact, there are 100 million of them in each of your eyes. But rods don’t play much of role in colour vision. They do play a big role in helping you see when it’s dark.

When light hits a rod cell, it causes a chemical, rhodopsin, that’s contained within the rod cells to change shape. When it does that, the rod sends signals to the brain that say: “hey, there’s light here.”
Cone cells are shaped like elephants….I’m kidding, they’re cones. and they are larger than rods. There are also far fewer of them: you only have have 7 million cones in each eye, and most of them are concentrated in one region of the retina called the “macula”, which is the part that produces the sharpest vision.

Cone cells aren’t as sensitive as rod cells, but they let you see colour. Most people have three different kinds of cone cells covering the retina.

They work in the same way as rod cells, but their shape changing chemicals are only sensitive to red, green, or blue light.

You see red when only the red cones are activated. You see blue when the blue cones are stimulated, and you see yellow when the red and green cones are stimulated.

Now there’s light on the back of the retina, how does the brain turn that into an image. Well, your brain gets its wires crossed. But in a good way.

Behind your eyes, the optic nerves, which takes signals from the retina to the brain cross paths. There they split, and the bundle of nerve fibres for the left side of each retina goes to the left side of the brain, and the same for the right side.
The brain then knows what’s on the left side of each eye, what’s on the right side, and what’s in the middle, which is probably what you’re looking at in the first place, and so it can combine that into an image.

This all happens in the visual cortex, a section at the very back of your brain. So everything in front of your nose is processed in the back of your head. Which is a bit strange.

But our two eyes have allowed humanity to be the best pupils of the world around us. So take care of them, try not to poke them too often, and enjoy what they have to show us.


Symptoms

Retinitis pigmentosa usually starts in childhood. But exactly when it starts and how quickly it gets worse varies from person to person. Most people with RP lose much of their sight by early adulthood. Then by age 40, they are often legally blind.

Because rods are usually affected first, the first symptom you may notice is that it takes longer to adjust to darkness (called “night blindness). For example, you may notice it when you walk from bright sunshine into a dimly lit theater. You may trip over objects in the dark or not be able to drive at night.

You may lose your peripheral vision at the same time or soon after your night vision declines. You may get "tunnel vision," which means you can’t see things to the side without turning your head.

In later stages, your cones may be affected. That will make it harder for you to do detail work, and you may have trouble seeing colors. It’s rare, but sometimes the cones die first.

You might find bright lights uncomfortable -- a symptom your doctor may call photophobia. You also may start to see flashes of light that shimmer or blink. This is called photopsia.


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The visual system is unique as much of visual processing occurs outside the brain within the retina of the eye. The previous chapter described how the light-sensitive receptors of the eye convert the image projected onto the retina into spatially distributed neural activity in the first neurons of the visual pathway (i.e., the photoreceptors). Within the retina, the receptors synapse with bipolar and horizontal cells, which establish the basis for brightness and color contrasts. In turn, the bipolar cells (the 2° visual afferent) synapse with retinal ganglion cells and amacrine cells, which enhance contrast effects that support form vision and establish the basis for movement detection. The information from the eye is carried by the axons of the retinal ganglion cells (the 3° visual afferent) to the midbrain and diencephalon. This chapter will provide more information about visual pathway organization and the visual processing that occurs within the brain.

15.1 The Visual Pathway from Retina to Cortex

As noted previously in the somatosensory sections, all sensory information must reach the cerebral cortex to be perceived and, with one exception, reach the cortex by way of the thalamus. In the case of the visual system, the thalamic nucleus is the lateral geniculate nucleus and the cortex is the striate cortex of the occipital lobe.

Figure 15.1
The visual pathway with the course of information flow from the right (green) and left (blue) hemifields of the two eye's visual fields.

The axons of the 3° visual afferents (the retinal ganglion cells) form the optic nerve fiber layer of the retina on their course to the optic disc. At the optic disc, the 3° visual afferents exit the eye and form the optic nerve. The fibers of the optic nerve that originate from ganglion cells in the nasal half of the retina (i.e., the nasal hemiretina) decussate in the optic chiasm to the opposite optic tract (Figure 15.1). Consequently, each optic tract contains retinal ganglion cell axons that originate in the nasal half of the contralateral retina and the temporal half of the ipsilateral retina. Recall that the ipsilateral temporal hemiretina and the contralateral nasal hemiretina have projected on them the images of corresponding halves of their visual fields. For example, the temporal (left) hemiretina of left eye and the nasal (left) hemiretina of right eye both have projected on them the right halves of their respective visual fields. Consequently, each optic tract has within it axons representing the contralateral half of the visual field.

The axons in the optic tract terminate in four nuclei within the brain (Figure 15.2):

  • the lateral geniculate nucleus of the thalamus - for visual perception
  • the superior colliculus of the midbrain - for control of eye movements
  • the pretectum of the midbrain - for control of the pupillary light reflex and
  • the suprachiasmatic nucleus of the hypothalamus - for control of diurnal rhythms and hormonal changes.

Figure 15.2
The inferior surface of the brain illustrating the visual pathway. The termination sites of the retinal ganglion cell axons in three nuclei that are not considered a part of the visual pathway are also illustrated. They include the hypothalamus, pretectum and the superior colliculus.

The Lateral Geniculate Nucleus

The vast majority of optic tract fibers terminate on neurons in the lateral geniculate nucleus (LGN) of the thalamus (Figure 15.3A).

Like the retina, the lateral geniculate nucleus is a laminated structure, in this case, with six principal layers of cells (Figure 15.3B).

  • The largest cells form the deepest two (magnocellular) layers
  • Smaller cells form the upper four (parvocellular) layers
  • Thin layers of the smallest cells (i.e., the koniocellular neurons) are interposed between these principal layers.

The optic tract fibers (3° visual afferents) from each eye synapse in different layers of the LGN. Consequently, each LGN neuron responds to stimulation of one eye only.

Figure 15.3
Structures of the visual pathway (A). The neurons of the lateral geniculate nucleus form 6 layers that are visible when stained for Nissl substance (B). The magnocellular layers (1 and 2) appear darker as the cells in these layers are larger and contain more Nissl substance than the cells in the parvocellular layers (3 through 6).

The functional properties of LGN neurons are similar to those of retinal ganglion cells.

The LGN neurons are monocular (i.e., respond to stimulation of one eye only) and have concentric (center-surround) receptive fields. The LGN neurons are segregated into three major groups:

  • The neurons in the magnocellular layers (mLGN cells)
    • process M-retinal ganglion cell inputs
    • behave like M-retinal ganglion cells
    • have relatively large center-surround receptive fields
    • are color insensitive
    • are most sensitive to movement of visual stimuli
    • process P-retinal ganglion cell inputs
    • behave like P-retinal ganglion cells
    • have relatively small center-surround receptive fields
    • are color sensitive
    • are well suited for detecting contrasts that form the basis for shape/form discrimination.
    • process P-retinal ganglion cell inputs
    • behave like P-retinal ganglion cells
    • have the smallest concentric receptive fields
    • have stronger color sensitivity than P-retinal ganglion cells
    • are well suited for detecting colors that aid in shape/form discrimination.

    The axons of these different types of LGN neurons terminate in different layers or sublayers of the primary visual cortex.

    The primary visual cortical receiving area is in the occipital lobe. The primary visual cortex is characterized by a unique layered appearance in Nissl stained tissue.

    Figure 15.4
    Nearly the entire caudal half of the cerebral cortex is dedicated to processing visual information. A lateral view of the left cerebral hemisphere (A). A view of the medial surface of the right hemisphere (B). The primary motor cortex (i.e., the precentral gyrus), and the primary somatosensory receiving area (i.e., the postcentral gyrus) are represented in red and blue, respectively. The numbers provide the Brodmann Area designation.

    Consequently, it is called the striate cortex. It includes the calcarine cortex, which straddles the calcarine fissure, and extends around the occipital pole to include the lateral aspect of the caudal occipital lobe (Figure 15.4, Area 17).

    Figure 15.5
    The course of the optic radiations from the lateral geniculate nucleus of the thalamus to the striate cortex of the occipital lobe is illustrated in a lateral view of the left side of the brain.

    The LGN neurons (4° visual afferents) send their axons in the internal capsule to the occipital lobe where they terminate in the striate cortex (Figure 15.5).

    • The LGN axons fan out as the optic radiations of the internal capsule and travel through the temporal, parietal and occipital lobes.
    • The LGN axons in the sublenticular segment of the optic radiations pass below the lenticular nuclei, loop around the inferior horn of the lateral ventricle within the temporal lobe and swing posteriorly to form Meyer’s loop.
      • Once around the inferior horn, they travel up to the inferior bank of the striate cortex, where they terminate.

      The striate cortex (Figure 15.6) is considered to be the primary visual cortex or V1, as

      • most LGN axons terminate in V1
      • all V1 neurons respond to visual stimuli exclusively
      • ablating V1 results in blindness
      • electrical stimulation of V1 elicits visual sensations.

      The striate cortex is involved in the initial cortical processing of all visual information necessary for visual perception and its damage results in loss of vision in the contralesional hemifield.

      Figure 15.6
      The topographic map of the left halves of the visual fields in the medial aspect of the right striate cortex. Note that the neurons representing the visual field center extend around the occipital pole into the lateral surface of the occipital lobe. This results in a disproportionate representation of the central field when compared to the cortical area representing the peripheral visual field.

      The color (kLGN), shape (pLGN) and movement (mLGN) information from the thalamus are sent to different neurons within V1 for further processing in V1 and then sent onto different areas of the extrastriate visual cortex.

      Figure 15.7
      The responses of a "shape-form" type primary visual cortex neuron is recorded while a light bar is flashed on and off the screen. For each of the frames, the light bar has a different orientation. The neuron displays a preference (i.e., produces a maximal response) for a light bar centered and parallel to the long axis of the receptive field.

      V1 blob cells : Some V1 cells resemble kLGN neurons. They are

      • monocular (i.e., respond to stimulation of one eye only).
      • color sensitive.
      • characterized by small, concentric receptive fields.
      • found in clusters (.e., blob cells).
      • a special target of the kLGN axon terminals.

      The P-stream information processed by the V1 blob cells is used in color perception, color discrimination and the learning and memory of the color of objects. The blob cells are the "color" processing cells of V1.

      V1 interblob cells: Most V1 interblob cells are

      • binocular (i.e., respond to stimulation of either eye).
      • not color sensitive.
      • characterized by elongated (rectangular-shaped) receptive fields that may or may not have a center-surround type organization.
      • found around the clusters of color-sensitive V1 blob cells.
      • exhibit ocular dominance (i.e., respond best to stimulation of a preferred eye).
      • exhibit orientation specificity (i.e., respond best when the stimulus is oriented in a particular plane).

      Location specific V1 interblob cells: One subset of V1 interblob cells responds best when the stimulus is in a specific location of the receptive field (i.e., they also exhibit location specificity).

      The P-stream information processed by the V1 interblob cells that exhibit orientation and location specificity but are not motion sensitive is used in object perception, discrimination, learning and memory or in spatial orientation. These interblob cells are the "shape/form" processing cells and the "location" processing cells of V1.

      Movement sensitive V1 interblob cells: A second subset of interblob cells respond best to moving stimuli (i.e., exhibit movement sensitivity, Figure 15.8) without a preference for the direction of movement.

      Figure 15.8
      The responses of a "motion sensitive" primary visual cortex neuron recorded in response to movement of a light bar across the neuron's receptive field from left to right.

      Figure 15.9
      The responses of a "motion sensitive" primary visual cortex neuron recorded in response to movement of a light bar across the neuron's receptive field. The neuron responds vigorously to movement in one direction (i.e., from left to right as in Figure 15.8) and poorly to movement in the opposite direction (i.e., from right to left). Consequently, this neuron exhibits directional sensitivity.

      Direction specific V1 interblob cells: A third subset displays a preference for movement in a particular direction (i.e., some also exhibit directional sensitivity, Figure 15.9).

      The M-stream of information processed by the motion sensitive V1 interblob cells is used to detect object movement and direction/velocity of movement and to guide eye movements. These motion-sensitive interblob cells are the "motion detecting” cells of V1.

      Extrastriate Visual Cortex. The extrastriate cortex includes all of the occipital lobe areas surrounding the primary visual cortex (Figure 15.4, Areas 18 & 19). The extrastriate cortex in non-human primates has been subdivided into as many as three functional areas, V2, V3, and V4. The primary visual cortex, V1, sends input to extrastriate cortex and to visual association cortex. The information from the “color”, “shape/form”, "location" and “motion” detecting V1, neurons are sent to different areas of the extrastriate cortex (Figure 15.10).

      Damage to extrastriate cortex does not result in a “simple loss of vision” rather it results in higher order visual perceptual deficits including the failure to recognize objects, colors and/or movement of objects.

      Figure 15.10
      The flow of visual information from the primary visual cortex to other cortical areas depends on the type of information being processed. Information used to locate objects and detect their motion is sent to more superior cortex (a.k.a. the dorsal stream). Information necessary to detect, identify and use color and shape information is sent to inferior cortical areas (a.k.a., the ventral stream).

      Visual Association Cortex . The visual association cortex extends anteriorly from the extrastriate cortex to encompass adjacent areas of the posterior parietal lobe and much of the posterior temporal lobe (Figure 15.4, Areas 7, 20, 37 & 39). In most cases, these areas receive visual input via the extrastriate cortex, which sends color, shape/form, location and motion information to different areas of the visual association cortex (Figure 15.10).

      The Dorsal Stream : The neurons in the parietal association cortex and superior and middle temporal visual association cortex (Areas 7 and 39 and the superior part of Area 37 in Figure 15.4) have binocular receptive fields and process P-channel information about object location and M-channel information about object movement.

      These dorsally located visual association neurons are responsible for producing our sense of

      • spatial orientation
      • binocular fusion/depth perception
      • the location, the movement and the movement direction and velocity of objects in space.

      The dorsal stream processes information about the “where” of the visual stimulus (Figure 15.10).

      Damage the dorsal visual association cortex results in deficits in spatial orientation, motion detection and in guidance of visual tracking eye movements.

      The Ventral Stream : The neurons in the inferior temporal visual association cortex (Area 20 and the inferior part of Areas 37 & 39 in Figure 15.4) process P-channel information about object color and form.

      These ventrally located visual association neurons are responsible for processing information necessary for our abilities to

      • recognize objects and colors
      • read text and
      • learn and remember visual objects (e.g., words and their meanings)

      This ventral stream processes information about the “what” of the visual stimulus (Figure 15.10).

      Damage to the inferior visual association cortex produces deficits in complex visual perception tasks, attention and learning/memory.

      15.2 Retinotopic Organization in the Visual Pathway

      The topographic (spatial) relationships of retinal neurons are maintained throughout the visual system, which preserves the retinotopic map of the visual world. That is, the retina is mapped onto the LGN and striate cortex in an organized (topographic) fashion. Consequently, neighboring parts of retina project to neighboring parts of LGN and neighboring parts of LGN project to neighboring parts of the striate cortex. This retinotopic organization in the visual pathway results in a spatial representation of the visual field in the LGN and visual cortex.

      Spatial Representation of the Retinal Image

      You should recall the following regarding the spatial representation of the retinal image within the visual pathway.

      • The optic image on the retina is upside-down and left-right reversed.
      • The monocular visual fields of the two eyes overlap partially to form the binocular visual field .
      • The temporal hemiretina of one eye and the nasal hemiretina of the other eye have projected on them the images of corresponding halves of their visual fields (Figure 15.1). For example, the temporal (left) hemiretina of left eye and the nasal (left) hemiretina of right eye both have projected on them the right half of the visual fields of each eye.
      • Beyond the optic chiasm, the corresponding visual hemifields of the two eyes are represented in the contralateral side of the visual pathway (Figure 15.1). For example, the left hemifield of both eyes are represented in the right optic tract, right lateral geniculate nucleus, right optic radiations and right striate cortex.
      • The fibers of the optic radiation fan out into the temporal, parietal and occipital lobes on their course to the striate cortex. Those forming the sublenticular optic radiations carry information about the superior hemifield, whereas those forming the retrolenticular optic radiations carry information about the inferior hemifield (Figure 15.5). The optic radiation fibers traveling the most direct course back to the striate cortex carry information about the central visual field.
      • There are many more receptor cells in the fovea and many more bipolar and ganglion cells in the macula than in the periphery of the retina. Consequently, the central visual field is disproportionately represented in the visual system. That is, more visual receptors, more optic nerve fibers and more LGN and cortical neurons are involved in processing and carrying information about that portion of the retinal image representing the center of the visual field.

      Visual field defects are areas of loss of vision in the visual field. Visual field defects are detected by perimetry testing, during which the patient fixates his eyes on a target and his ability to detect a small object in specific positions in space is determined.

      Figure 15.11
      The binocular visual field (top panel), perimetry testing results for the monocular visual fields (middle panel) and a simplified version of the monocular visual fields (bottom panel) of a person with normal vision. In this panel, the blind spot is illustrated as a dark oblong spot, whereas the central visual field is illustrated as a larger yellow circle.

      Figure 15.11 illustrates perimetry test results for the two eyes of someone with normal vision. The bottom panel of Figure 15.11 is a simplified illustration of the monocular visual fields used in the following examples of visual field defects. A visual field defect provides clues to the structure(s) affected. That is, the area(s) of visual field loss and eye(s) exhibiting the visual field loss offer clues about the site of the damage. The following examples of visual field losses should help you determine how well you can utilize what you have learned thus far about the visual system.

      Figure 15.12
      Ophthalmoscope examination of the fundus detects an abnormality in the nasal hemiretina in the left eye of a diabetic patient. Notice that the fundus of the patient's left eye appears to the right, just as it appears on the right side of the physician viewing the fundus.

      Symptoms: The patient is having his semiannual physical examination. As he is diabetic, the physician examines his retinas and performs a confrontation test of his visual fields. An abnormality is detected in his left fundus (Figure 15.12) but the confrontational field test detects nothing.

      Perimetry testing is requested.

      Perimetry Test Results: The results indicate the right eye's visual field is normal and that there is peripheral a scotoma (i.e., loss of vision that does not follow the boundaries of the visual field quadrants) in the left eye's temporal hemifield (Figure 15.13).

      Figure 15.13
      The fundus of each eye as seen by the physician (A). The perimetry map of the monocular visual fields as viewed by the patient (B). The perimetry test result for the left eye indicates a small loss of vision in the temporal hemifield. The scotoma appears smaller in B as the view of the retina in A is limited to approximately 35 degrees, which extends from the nasal edge of the macula to slightly beyond the temporal edge of the optic disc.

      Side & Retinotopicity of damage: The visual loss

      • is limited to the left eye
      • is in the temporal (left) hemifield
      • is associated with retinal abnormalities in the nasal hemiretina of the left eye

      So you conclude that the visual defect involves

      • retinal damage in the left eye
      • damage located in the nasal half of the left retina (Figure 15.14, Lesion 1)
      • damage related to the patient's diabetes - diabetic retinopathy

      Figure 15.14
      This cartoon illustrates the central visual pathway (right panel) and the effects of lesions in the pathway (left panel). The numbered lesions in the right panel produce the correspondingly numbered visual field defects in the left panel.

      Retinal Damage: A defect involving only the visual field of one eye indicates possible damage in the retina or optic nerve. If the visual loss is confined to one eye, it is called a monocular visual field defect. Often retinal lesions are small and do not follow the boundaries of the visual field quadrants. Such a visual field disorder is called a scotoma. A retinal visual field defect is most severe when vision in the central field is affected, as in the case of macular degeneration. In macular degeneration, the patient will report difficulty reading and seeing clearly and visual field testing will demonstrate that the patient has a central scotoma (i.e., is blind in the visual field center).

      Figure 15.15
      The perimetry test results indicates a loss of vision over most of the visual field of the left eye - with no loss in the right eye's visual field. Notice that the central visual field for the left eye is represented by a black spot, indicating a loss of central field vision.

      Symptoms: The patient complains of a sudden headache and loss of vision in his left eye. Ophthalmoscope examination does not reveal abnormalities in the left eye 1 . However, confrontation testing indicates a severe loss of vision in the left eye.

      The patient is referred for immediate neuroradiographic tests and perimetry testing.

      Perimetry Test Results: The results indicate the right eye's visual field is normal and that there is a large visual loss encompassing nearly all of the left eye's visual field (Figure 15.15).

      Side & Retinotopicity of damage: The visual loss

      • does not appear to relate to changes in the retina of the left eye
      • is limited to the left eye
      • encompasses nearly the entire the visual field of the left eye

      So, you conclude that the visual defect is

      • retrobulbar (beyond the retina or eye) (Figure 15.14, Lesion 2)
      • probably limited to optic nerve damage (only one eye affected)

      Neural imaging results indicate an aneurysm on the left ophthalmic artery, which is compressing the left optic nerve (Figure 15.16). Compression of the nerve prevents action potentials from the retina to travel to the lateral geniculate nucleus of the thalamus. Long-term compression may damage the nerve, however, of greater concern is the potential rupture of the aneurysm, which could cause extensive brain damage.

      Figure 15.16
      A view of the inferior surface of the brain illustrating an aneurysm in the left ophthalmic artery, which is compressing the left optic nerve.

      Optic Nerve Damage: Each optic nerve contains the axons of retinal ganglion cells from one eye, e.g., the right nerve from the right eye. Damage to one optic nerve will produce a monocular visual field defect. Destruction of one optic nerve (e.g., crushed by a tumor on the orbital surface of the frontal cortex) will result in the total loss of vision in the ipsilesional eye.

      Figure 15.17
      The perimetry test results for Example 3 indicate a bitemporal hemianopia (i.e., a bilateral visual defect involving the temporal hemifields of both eyes). Notice that only the temporal halves of the two central areas exhibit a visual loss (i.e., appear as dark hemicircles).

      Symptoms: At his annual physical exam, the patient complains of a general malaise and changes in his vision that he noticed while playing soccer. He said he was often "blindsided" on the playing field because he "couldn't see players approaching him from the side". Ophthalmoscope examination does not reveal abnormalities in either eye 2 . Confrontation field testing indicates a constriction of the temporal hemifields of both eyes. The patient is referred for neuroradiographic tests and perimetry testing.

      Perimetry Test Results: The results indicate a bitemporal hemianopia, i.e., loss of vision in the temporal hemifields of both eyes (Figure 15.17).

      Side & Retinotopicity of damage: The visual loss

      • is not related to changes in the retina of either eye
      • involves vision in both eyes
      • encompasses only the temporal hemifields

      You conclude that the visual field defect is related to damage that

      Neural imaging results (Figure 15.18) indicate a pituitary adenoma that is compressing the optic chiasm. Compression of the decussating nerve fibers prevents action potentials from the nasal hemiretina to reach the contralateral lateral geniculate nucleus of the thalamus. As the tumor grows larger it will crush the optic chiasm, destroying it and eventually compromising the remaining optic nerve fibers.

      Figure 15.18
      A view of the inferior surface of the brain illustrating a pituitary tumor, which is compressing the optic chiasm.

      Optic Chiasm Damage: The fibers of the optic nerve that originate from ganglion cells in the nasal half of the retina decussate in the optic chiasm to the opposite optic tract (Figure 15.1). The crossing fibers of the optic chiasm may be crushed by a pituitary tumor. Damage to the optic chiasm produces a unique form of visual field deficit, a bitemporal hemianopia (Figure 15.17). Recall that the fibers of the optic chiasm carry information about objects in the temporal hemifields of both eyes (i.e., the right hemifield of the right eye and the left hemifield of the left eye). Consequently section of the optic chiasm produces a visual loss in only the temporal half of the visual field of each eye. When the patient views the world out of both eyes, the boundary of his binocular visual field is narrower than normal.

      Figure 15.19
      The perimetry test results indicate a right homonymous hemianopia (i.e., a binocular visual defect involving the right hemifields of both eyes) with macular sparing (i.e., central field vision was not affected).

      Symptoms: A patient is brought to the emergency room complaining of a severe headache and nausea. He is conscious and coherent when examined in the ER. Ophthalmoscope examination does not reveal abnormalities in either eye. Confrontation field testing indicates a visual loss in the right hemifield of both eyes.

      The patient is referred for neuroradiographic tests and perimetry testing.

      Perimetry Test Results: The results indicate a right homonymous hemianopia with macular sparing (Figure 15.19).
      Side & Retinotopicity of damage: The visual loss

      • is not related to changes in the retina of either eye
      • involves field losses for both eyes
      • involves the right hemifields
      • is homonymous or congruent
      • spares the central visual field

      You conclude that the visual field defect is related to damage that

      • is retrobulbar (beyond the retina)
      • is retrochiasmatic or postchiasmatic (beyond the optic chiasm)
      • involves the left calcarine cortex
      • may involve hemorrhage from a branch of the left posterior cerebral artery
      • spared the more caudal and lateral parts of the striate cortex, which receives collateral blood flow from branches of the middle cerebral artery

      Neural imaging results indicate injury to the rostral half of the left calcarine cortex, which receives blood from the left posterior cerebral artery (Figure 15.20). Recall that the rostral calcarine cortex processes information from the visual field periphery, whereas the caudal and lateral striate cortex process information derived from the visual field center.

      Figure 15.20
      The perimetry test results indicate a right homonymous hemianopia with macular sparing. The medial and inferior portions of the occipital lobe receives blood from branches of the posterior cerebral artery.

      Calcarine Cortex Damage. An infarct created by obstruction of, or a hemorrhage in, branches of the posterior cerebral artery may result in damage to the rostral calcarine cortex. Damage to the calcarine cortex on one side may produce a binocular, contralateral homonymous hemianopia with macular sparing (Figure 15.20). A collateral blood supply from branches of the middle cerebral artery is believed to spare the cortical neurons in the caudal and lateral regions of the striate cortex, which receive information from the macular area.

      Figure 15.21
      The cortical areas involved in color perception and face recognition are illustrated in the left hemisected brain with cerebellum removed (A). Distribution of the major branches of the anterior and posterior cerebral arteries viewed on the inferior and medial surfaces of the brain with the cerebellum removed (B). The location of the lesion is colored red.

      Symptoms: A patient, who is stabilized after suffering a stroke two months earlier, is referred to a neuro-ophthalmologist for evaluation. The patient does not appear to be blind but has problems with processing visual information. For example, the patient cannot describe the color of an object presented to him or recognize faces. He has normal spatial orientation and motion detection.

      The patient is referred for perimetry testing.

      Perimetry Test Results: The results indicate no consistent loss of vision. However, it is difficult to obtain consistent results because the patient tires easily and his attention appears to wander.

      Side & Retinotopicity of damage: The patient

      • is not blind in either eye
      • does not have deficits in detecting the location or movement of objects
      • does not exhibit the symptom of "neglect" (i.e., visual inattention)
      • exhibits deficits in higher visual processing involving color and object recognition

      You conclude that the neurological defect is

      • not related to damage in the visual pathway from the eye to the striate cortex
      • not related to damage in the middle or superior temporal gyrus
      • not related to damage in the parietal lobe
      • related to damage in the inferior temporal gyrus (Figure 15.21)
      • involving branches of the posterior cerebral artery that supply the inferior temporal gyri

      Neural imaging results indicate damage to the caudal portion of the inferior temporal lobe, which normally receives blood from branches of the posterior cerebral artery.

      Extrastriate or Association Cortex Damage: While destruction of the primary visual cortex produces blindness in the contralesional hemifield, damage to cortical areas surrounding the striate cortex does not Instead, they may produce profound deficits in the higher order-processing of visual information. For example, bilateral damage to a small area of the inferior temporal gyrus (Figure 15.21) produces a loss in the ability to recognize faces. Damage to more superior areas of the temporal lobe (area 39 in Figure 15.4) produces an inability to recognize or comprehend written words and/or passages. Damage to areas in the parietal cortex may result in the inability to see motion (i.e., a moving object will be seen in “frames’’ in one place at one point in time and at another place in a following period of time). The object does not appear to move rather it appears to have jumped from one place to the next. Damage to large areas involving the posterior parietal cortex and superior temporal cortex may result in the symptom of "neglect", wherein objects in parts of the visual field are ignored or denied existence.

      In this chapter, you have learned how the visual system is organized in the brain. You have learned that stimulus features extracted by the retinal neurons (color, brightness contrast, movement) are kept segregated in separate “information channels” and processed in parallel by different cells at all levels of the visual system. Information coded and carried by one million retinal ganglion cells are distributed to hundreds of millions of cortical neurons in the occipital, parietal and temporal lobes. The perception of a coherent visual image is recomposed out of these fragments of information by the simultaneous activation of large areas of cortex. You have also learned how the spatial representation of the visual image is maintained by the retinotopic organization of the visual system and learned how this information is useful in determining the location and extent of damage to the visual system by examining the visual fields. Finally, you have learned that neuronal responses in visual cortex exhibit plasticity at different time scales, short term (as adaptation and dynamics) and long term (as learning) – this plasticity allows visual cortex to construct an accurate picture of the world that can rapidly adapt to match the changes in the environment.

      Which of the following are characteristic of the primary visual cortex "blob" neurons? They:

      A. are binocular and exhibit ocular dominance.

      B. have color opponent receptive fields.

      C. require a specific stimulus orientation.

      D. have elongated receptive fields.

      E. synapse with magnocellular lateral geniculate neurons.

      Which of the following are characteristic of the primary visual cortex "blob" neurons? They:

      A. are binocular and exhibit ocular dominance. This answer is INCORRECT.

      B. have color opponent receptive fields.

      C. require a specific stimulus orientation.

      D. have elongated receptive fields.

      E. synapse with magnocellular lateral geniculate neurons.

      Which of the following are characteristic of the primary visual cortex "blob" neurons? They:

      A. are binocular and exhibit ocular dominance.

      B. have color opponent receptive fields. This answer is CORRECT!

      C. require a specific stimulus orientation.

      D. have elongated receptive fields.

      E. synapse with magnocellular lateral geniculate neurons.

      Which of the following are characteristic of the primary visual cortex "blob" neurons? They:

      A. are binocular and exhibit ocular dominance.

      B. have color opponent receptive fields.

      C. require a specific stimulus orientation. This answer is INCORRECT.

      D. have elongated receptive fields.

      E. synapse with magnocellular lateral geniculate neurons.

      Which of the following are characteristic of the primary visual cortex "blob" neurons? They:

      A. are binocular and exhibit ocular dominance.

      B. have color opponent receptive fields.

      C. require a specific stimulus orientation.

      D. have elongated receptive fields. This answer is INCORRECT.

      E. synapse with magnocellular lateral geniculate neurons.

      Which of the following are characteristic of the primary visual cortex "blob" neurons? They:

      A. are binocular and exhibit ocular dominance.

      B. have color opponent receptive fields.

      C. require a specific stimulus orientation.

      D. have elongated receptive fields.

      E. synapse with magnocellular lateral geniculate neurons. This answer is INCORRECT.

      Make the best match between the below listed condition and the visual field defect. Match: occlusional of the left posterior cerebral artery

      A. Contralesional superior quadrantanopia with macular sparing

      B. Contralesional inferior quadrantanopia with macular sparing

      C. Contralesional homonymous hemianopia with macular sparing

      D. Bitemporal hemianopia

      E. Inability to recognize objects or colors

      Make the best match between the below listed condition and the visual field defect. Match: occlusional of the left posterior cerebral artery

      A. Contralesional superior quadrantanopia with macular sparing This answer is INCORRECT.

      B. Contralesional inferior quadrantanopia with macular sparing

      C. Contralesional homonymous hemianopia with macular sparing

      D. Bitemporal hemianopia

      E. Inability to recognize objects or colors

      Make the best match between the below listed condition and the visual field defect. Match: occlusional of the left posterior cerebral artery

      A. Contralesional superior quadrantanopia with macular sparing

      B. Contralesional inferior quadrantanopia with macular sparing This answer is INCORRECT.

      C. Contralesional homonymous hemianopia with macular sparing

      D. Bitemporal hemianopia

      E. Inability to recognize objects or colors

      Make the best match between the below listed condition and the visual field defect. Match: occlusional of the left posterior cerebral artery

      A. Contralesional superior quadrantanopia with macular sparing

      B. Contralesional inferior quadrantanopia with macular sparing

      C. Contralesional homonymous hemianopia with macular sparing This answer is CORRECT!

      There will be macular sparing because the caudal and lateral striate cortex receives a collateral blood supply from branches of the middle cerebral artery.

      D. Bitemporal hemianopia

      E. Inability to recognize objects or colors

      Make the best match between the below listed condition and the visual field defect. Match: occlusional of the left posterior cerebral artery

      A. Contralesional superior quadrantanopia with macular sparing

      B. Contralesional inferior quadrantanopia with macular sparing

      C. Contralesional homonymous hemianopia with macular sparing

      D. Bitemporal hemianopia This answer is INCORRECT.

      E. Inability to recognize objects or colors

      Make the best match between the below listed condition and the visual field defect. Match: occlusional of the left posterior cerebral artery

      A. Contralesional superior quadrantanopia with macular sparing

      B. Contralesional inferior quadrantanopia with macular sparing

      C. Contralesional homonymous hemianopia with macular sparing

      D. Bitemporal hemianopia

      E. Inability to recognize objects or colors This answer is INCORRECT.


      What is the direction of the processing of light by the (human) retina and how does it happen? - Biology



      The human eye is a complex organ that contains many cells, ligaments and other structures that function together to focus upon an object once light enters the eye. When light does enter the eye, different things happen. For example, some muscles relax while performing a task, while ligaments are pulled tight.

      Definition

      When an eye focuses on an object, it is called accommodation. According to Think Quest, accommodation is defined as changing the “focal length of the lens by changing the curvature of the eye lens.” Accommodation allows images at different distances to be focused on the retina.

      Focusing Near

      When the eye focuses on a near object, the eye must accommodate to be able to see the object clearly. The ciliary muscle contracts, which releases tension on the ligaments that suspend the eye. As a result, both lens surfaces become more curved and the eye thus focuses on the nearby object.

      What Happens

      There are several things that happen when the eye focuses on a local object, including the ciliary muscle contracting and the relaxation of the suspensory ligament. Additionally, the crystalline lens becomes thicker, the focal length shortens and light rays converge earlier thus creating the image on the retina. According to the Physics Classroom, “the reduction in focal length will cause more refraction of light and serve to bring the image back closer to the cornea/lens system and upon the retinal surface.”

      More Effort

      According to Dr. Ted Montgomery, the closer an object is to the eyes, “the more effort the ciliary muscles must exert for the eyes to focus clearly on that object.” Because of this, more strain is placed on the intraocular muscles, which quite often produces headaches. To help prevent strain on the eyes and even headaches, one should sit up straight when writing, keep reading material away from the eyes when reading and keep an arm’s distance away when sitting at a computer.

      Nearpoint Stress

      Nearpoint stress is defined as stress on the eyes due to extended periods of near work, including reading, surfing the Internet and sewing. Because the eyes work so hard to focus on the near work, by the time you look away to rest your eyes, farther objects appear blurry and would take longer to come into focus. Symptoms of nearpoint stress include eye fatigue, headaches, blurred vision and even a poor ability to concentrate on tasks up close.


      Auditory Inhibition

      Lateral inhibition is thought to play a role in hearing and the auditory pathway of the brain. Auditory signals travel from the cochlea in the inner ear to the auditory cortex of the brain's temporal lobes. Different auditory cells respond to sounds at specific frequencies more effectively. Auditory neurons receiving greater stimulation from sounds at a certain frequency can inhibit other neurons receiving less stimulation from sounds at a different frequency. This inhibition in proportion to stimulation helps to improve contrast and sharpen sound perception. Studies also suggest that lateral inhibition is stronger from low to high frequencies and helps to adjust neuron activity in the cochlea.


      Watch the video: DHARIA - August Diaries by Monoir Lyrics (May 2022).