After studying this chapter, the student should be able to:
Describe the optical functions of the cornea and lens, problems that occur in focus, and the correction of these problems.
Describe the process of phototransduction from photon capture to neurotransmitter release.
Diagram the neural circuit of the retina, and outline the function of each major cell class.
List the central projection targets of retinal ganglion cells and describe the functions of these brain areas.
IMAGING & CAPTURING LIGHT
Vision begins with light passing through the cornea and lens, the optical elements that refract, focus, and transmit light to the innermost layer of the eye, the retina, the region that transduces light information to electrical signals and transmits them to the brain. Because the cornea is at the interface between air (index of refraction close to 1.0) and the corneal tissue (index of refraction about 1.38), the cornea does most of the focusing. The lens, with a slightly higher index of refraction than the aqueous humor (variable, but about 1.4 in its center), fine tunes the focus. Ciliary muscles modulate refraction by the lens, controlling focus. This process is called accommodation. Because the cornea and lens are converging and positive lenses, they project an inverted image on the retina.
The main structural elements of the eye are shown in Figure 11–1.
The anatomy of the eye. A. An axial cross-section of the eye. The outer surface of the eye is the sclera. Inside that is the choroid containing blood vessels that nourish the retina and pigment epithelium. Inside the choroid is the retina. The vitreous (from the Latin for glass) is a gel-like substance that fills the inside of the eye. The area of highest acuity in the eye is the macula lutea. Within the macula is the small area of ultra-high acuity found only in mammals and some birds, the fovea centralis. The optic disk is where the ganglion cell axons leave the optic nerve. There are no photoreceptors there, so it constitutes the “blind spot” in the retina. B. Close-up of the anterior portion of the eye. The cornea does approximately 70% of the focusing. Between the cornea and lens is the aqueous humor. Just in front of the lens is the pupil made by the iris. Pupil size is controlled by the ciliary muscle, which is driven by the ciliary nerve. C. How accommodation, the control of focus, works: The lens fine-tunes the focusing of light entering the eye. Light from a distance is refracted a small amount by the stretched, flat lens to strike the retina in focus. D. Light from a source nearby is refracted more by the relaxed, more convex lens to be focused on the retina. This is controlled by the third cranial nerve (CN), the oculomotor nerve. m., muscle. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy, 2nd ed. New York, NY: McGraw Hill; 2019.)
The eye is composed of 3 main layers that enclose 3 transparent structures. The outermost layer, composed of the cornea and sclera, is called the fibrous tunic. The middle layer, composed of the choroid, ciliary body, and iris, is called the vascular tunic (uvea). The inner layer is the retina, which obtains its blood supply from the choroid and retinal vessels. Within these layers are 3 transparent structures: (1) the aqueous humor, filling the anterior and posterior chambers between the lens and cornea; (2) the gelatinous vitreous humor (vitreous body), filling the bulk (80%) of the eyeball between the lens and the retina; and (3) the flexible lens. The overall structure of the eye is illustrated in the section view in Figure 11–1A.
Figure 11–1B shows a magnified section of the anterior portion of the eye. Approximately 70% of the focusing of the light is done at the cornea at the air–tissue interface. The lens fine-tunes this focus by changing its shape, illustrated in Figures 11–1C and 11–1D. The control of focus is called accommodation. The pupil is an adjustable hole in the iris that controls the amount of light entering the eye. The pupil size is controlled by the third cranial nerve, the oculomotor nerve. This nerve arises from 2 nuclei in the anterior mesencephalon (midbrain): the oculomotor nucleus and the Edinger-Westphal nucleus. The Edinger-Westphal nucleus projects to the eye via the ciliary ganglion as part of the parasympathetic system. It controls pupil constriction via the sphincter pupillae muscle and accommodation via the ciliary muscle. The oculomotor nucleus also controls eye movements (see later discussion).
The Formation of Images on the Retina
The optical elements of the eye are critical for normal vision, and thus, dysfunction, aging, or errors in development of these elements can require corrective lenses or surgery. Conditions affecting the eye include the following:
Opacities in the cornea or lens (cataracts) that block or scatter light, resulting in degradation of image quality.
Asphericity in the cornea reducing focusing quality, called astigmatism. There are 2 types of astigmatism: meridional and nonmeridional astigmatism. Meridional astigmatism is characterized by a corneal surface that is slightly cylindrical rather than spherical, making its focusing power in 1 axis different than off that axis. If, for example, the cornea/lens optical system is set for proper vertical but not horizontal focus, vertical lines can be resolved, but horizontal lines would be blurry. Nonmeridional astigmatism, in contrast, occurs when the corneal surface is irregular in a complex way such that there is not even a single axis of good focus.
Conditions that affect focus, such as myopia and hyperopia. The eye is said to be emmetropic if the match between the focusing power of the cornea and lens and the length of the eye is such that light from distant objects is correctly focused on the retina when the lens is in its flattest, lowest power state. During normal development, the growth of the eye matches changes in the eye’s optics, but errors in this process result in either myopia, where the length of the eye is too long for the front of the eye optics, or hyperopia, where it is too short (Figure 11–2). In myopia, the power of the cornea/lens system is too high for the length of the eyeball, so that myopes cannot focus on distant objects. However, myopes can focus on objects closer to the eyes than those with normal emmetropic eyes. A negative lens (Figure 11–2A, bottom) is used to reduce the cornea/lens power and achieve normal focus. In hyperopia, the cornea/lens system has insufficient power for the length of the eye. In mild cases, lens accommodation may allow distant objects to be focused, but then there is no remaining accommodative power to focus near objects. This is corrected with a positive lens (Figure 11–2B, bottom).
Presbyopia (literally “old eye”) arising during aging, in which the lens hardens and can no longer be made to bulge to increase its optical power. If one is emmetropic prior to the onset of presbyopia, then distance vision, where the lens is flat, is normally unaffected, but lens power cannot be increased to see closer objects, requiring, for example, reading glasses. Someone who is not emmetropic prior to presbyopia onset may require different compensation lenses for distant versus close vision, such as bifocals.
Refractive error in the eye and its correction. A. In normal sight (top) the optics of the eye match its length, so that when the lens is at its flattest, parallel rays from very distant objects are focused on the retina. In myopia (middle), the eyeball grows too long for the eye’s optics, and distant parallel rays are focused in front of the retina, producing blurry vision at distance. Close objects may be in focus, however, because their diverging rays require more power in the lens. Hence, the popular name for myopia is “near-sightedness.” Myopia is corrected with a negative curvature (concave) lens (bottom). B. In hyperopia, the eyeball is too short for the eye’s optics, and parallel rays from distant objects are focused behind the retina. Normally people with hyperopia will accommodate to see distant objects. This leaves no accommodation for near objects, however, so they are called “far-sighted.” Hyperopia is corrected with a positive (convex) lens (bottom). (Reproduced with permission from Widmaier EP, Raff H, Strang KT. Vander’s Human Physiology, 11th ed. New York, NY: McGraw Hill; 2008.)
Our eyes move continually. Eye movements can be voluntary or involuntary and are essential for acquiring, fixating, and tracking visual stimuli. About 3 to 4 times a second, the eyes make large movements, called saccades, that shift the fovea to a new area of attention. The fovea is the small specific pit-like region of the retina, located within a disk called the macula that is involved in sharp central vision (see Figure 11–1).
Figure 11–3 shows eye movements recorded during free fixation of a photograph of a girl’s face. In between saccades, during fixation, our eyes make several types of small movements, called microsaccades, drift, and tremor, which are necessary for vision. Eye movements are controlled by 3 cranial nerves. The oculomotor nerve controls the majority of eye muscles, with the exception of the superior oblique, which is controlled by the trochlear nerve, and the lateral rectus, controlled by the abducens nerve.
The pattern of eye movements for an observer looking at the face of a young girl. Eye movements are characterized by a sequence of fixations lasting about one-quarter of a second followed by rapid eye movements called saccades to new location. Fixations tend to occur at points in the scene of particular interest, which in this case are the girl’s eyes and mouth. (Reproduced with permission from Yarbus AL. Eye Movements and Vision. New York, NY: Plenum Press; 1967.)
If images are artificially stabilized on the retina, after a few seconds, all vision disappears because the retina adapts to constant light and only responds to changes. The brain takes into account the eye movements it commands with the associated image movements so that when you are tracking a bird moving across the sky and the image on the retina is relatively stationary, your brain knows that the bird is moving because it knows your eyes are moving with it. When we move, the output of the vestibular system (the semicircular canals in the ear) is stimulated by self-movement. This signal is combined with visual information so that we perceive movement of ourselves rather than that of things around us.
Images transformed by the cornea and lens are projected onto the retina, the neural tissue in the innermost lining of the eye. The retina and optic nerve are derived from the optic vesicle of the prosencephalon of the neural tube and are considered part of the central nervous system (CNS) and brain. The retina is a component of the CNS that is located outside the skull or vertebral column, for the obvious reason of allowing light to be imaged by the transparent anterior eye components.
The retina is nourished by 2 main sources of vasculature. The first of these is the central retinal artery and vein, which enter through the optic nerve. These blood vessels ramify a capillary bed across the retinal surface everywhere except in the macular area of highest visual acuity. The other source of blood supply is the choroidal vasculature, which is just distal to the retinal pigment epithelium (RPE). These vascular structures are illustrated in Figure 11–4A. This figure also shows the macula lutea and fovea centralis, structures at the center of the retina that enable the highest visual acuity. The macula is blood vessel free and exhibits a high density of cones and rods. The fovea, in the center of the macula, has an ultra-high density of cones and is rod free. The fovea receives input from the central one-half degree of visual angle, which is about the size of the moon. The center of the fovea has only red and green cones, but no blue cones.
Detailed view of the optic disk, macula, fovea, and retina. A. A cross-section through the eye at the optic nerve head and fovea shows important structures of the eye. The central retinal artery and vein enter the eye from the optic nerve and produce the blood circulation in the choroid, located just distal to the retinal pigment epithelium. Below the optic nerve head is the central region of high acuity, the macula lutea. Within this region is the region of ultra-high acuity, the fovea centralis. B. A cross-section through the retina showing the 5 major cell types and their relationship to the surrounding tissues. (Reproduced with permission from McKinley MP, O’Loughlin VD. Human Anatomy, 3rd ed. New York, NY: McGraw Hill; 2012.)
A typical region of the retina outside the fovea is illustrated in Figure 11–4B. Because the retina more or less lines the inside of the spherical eyeball, vision scientists use the center of the eye as the main reference point and the terms proximal and distal to refer to cell and synaptic layers closer to and farther from, respectively, this center point. The most proximal illustrated structure is a capillary on the proximal surface of the retina (next to the vitreous) from the central retinal artery. Distal to this is the ganglion cell axon layer, then the retinal neurons and synaptic layers, the RPE, and finally, the choroid. Light passes through all the cell and synaptic layers before reaching the photoreceptor outer segments at the top of Figure 11–4. To prevent scattering, light not absorbed by the photoreceptor outer segments is absorbed by the dark RPE.
Two nonneural cell types are important in the function of the retina. Figure 11–5 shows, on the left, a photomicrographic cross-section of the retina stained for cell bodies rather than processes. This reveals the neural cell layers. On the right of the figure is a depiction that includes 2 important nonneural cells: the RPE cell, discussed earlier, and the Müller cell. Radial Müller cells are glia that extend throughout the entire radius of the retina. Their end feet form the inner limiting membrane at the vitreal surface.
Diagram of the layers of the retina from Bruch’s membrane at its outermost extent to the inner limiting membrane next to the vitreous. Layers with cell bodies include the outer nuclear layer containing photoreceptor somas, the inner nuclear layer containing the somas of horizontal, bipolar and amacrine cells, and the ganglion cell layer with somas of ganglion cells and some amacrine cells. The two major synaptic layers are the outer plexiform layer where photoreceptor terminals contact bipolar and horizontal cell dendrites, and the inner plexiform layer where bipolar cell terminals contact ganglion and amacrine cell dendrites. (Reproduced with permission from Riordan-Eva P, Augsburger JJ: Vaughan & Asbury’s General Ophthalmology, 19th ed. New York, NY: McGraw Hill; 2018.)
The relationship between the photoreceptor outer segments and the RPE is shown in Figure 11–6. Photoreceptor health and function are dependent on the RPE, which supplies vitamin A for production of retinal, the photon-absorbing molecule associated with the photoreceptor opsin. Lysosomal enzymes within the RPE also digest the rod outer segment tips that are constantly shed as their light-absorbing pigment is used up. Dark melanosomes within the RPE prevent scattered light and image blurring. Blindness in diseases such as retinitis pigmentosa (RP) stem from RPE dysfunction.
The retinal pigment epithelium (RPE). Photoreceptor health and function are dependent on the RPE. The RPE supplies vitamin A for production of retinal, the photon-absorbing molecule associated with the photoreceptor opsin. Lysosomal enzymes within the RPE also digest the constantly shed rod outer segment tips. Dark melanosomes within the RPE prevent scattered light and image blurring. Blindness in diseases such as retinitis pigmentosa stem from RPE dysfunction. RER, rough endoplasmic reticulum; SER, smooth endoplasmic reticulum.
Retinal Neurons: Organization & Function
There are 5 major classes of retinal neurons whose location and connectivity are illustrated in Figure 11–7. The initial process of seeing, as mediated by the retina, starts with the capture of light photons by photoreceptor cells, which are specific types of sensory neurons. Light capture controls the release of glutamate by the photoreceptors. This glutamate modulates the activity of bipolar and horizontal cells to which they are connected in the outer plexiform layer. Bipolar cells, in turn, activate amacrine and retinal ganglion cells in the inner plexiform layer. The result of this process is the conversion of the optical image to several neural images represented in the firing of different ganglion cell classes whose axons form the optic nerve and project to visual processing centers in the brain. This is discussed in more detail later.
The 5 major cell classes of the retina and their organization. This view shows the retinal cells in the orientation they occupy in the superior retina. The photoreceptor cell labels are C for cone and R for rod. Horizontal cells are labeled as H, and amacrine cells are labeled as A. The 3 types of bipolar cell are midget (MB), rod (RB), and flat bipolar (FB) cells. Two major ganglion cell classes are diffuse and midget, labeled DG and MG, respectively. Light passes through the inner retina (ganglion cell axons, then ganglion cells, and so forth, reaching the photoreceptor outer segments last, where the photons are absorbed). Photons not captured by photopigment molecules in the photoreceptors are absorbed by the pigment epithelium to prevent scattering and image blurring. Retinal processing involves a 3-neuron chain in the major throughput pathway, namely, photoreceptors, bipolar cells, and ganglion cells. Ganglion cells are the output of the retina via their axons that exit at the optic disk and make up the optic nerve. These axons are unmyelinated within the retina to avoid light scattering because light passes through the axon layer before reaching the photoreceptor outer segments. Horizontal cells modulate the signal from photoreceptors to bipolar cells. Amacrine cells modulate the signal from bipolar to ganglion cells. There are 3 main cell soma layers: the outer nuclear layer (photoreceptor somas), the inner nuclear layer (somas of horizontal, bipolar, and amacrine cells), and the ganglion cell layer. There are 2 major synaptic layers: the outer plexiform and inner plexiform layers. (Reproduced with permission from Dowling JE, Boycott BB: Organization of the primate retina: electron microscopy, Proc R Soc Lond B Biol Sci. 1966 Nov 15;166(1002):80-111.)
Retinal layers and cells. The retina is an ordered, layered, hierarchical structure with distinct cell body and synaptic layers. Starting from the most proximal layer at the vitreal surface (where light enters) is the optic nerve fiber layer. This layer contains the axons of retinal ganglion cells that will gather at the optic nerve head and exit the retina on their way to the optic chiasm and retinal recipient zones in the brain. Distal to that is the ganglion cell layer that contains the cell bodies of the retinal ganglion cells (2 types are shown: midget and diffuse). Within the ganglion cell layer are also several types of amacrine cells, which are interneurons that do not project to the brain (and are not shown in the ganglion cell layer in Figure 11–7). These are called “displaced” amacrine cells. Distal to the ganglion cell layer is the inner plexiform (plexiform = synaptic) layer, which contain the output terminals of bipolar cells that release glutamate onto the dendrites of amacrine and ganglion cells.
Distal to the inner plexiform layer is the inner nuclear layer that contains the cell bodies of bipolar (midget, rod, and flat bipolar), horizontal, and amacrine cells. Distal to that is the outer plexiform layer, which contains the photoreceptor terminals that synapse onto bipolar cell and horizontal cell dendrites. Beyond that is the outer nuclear layer containing the photoreceptor cell bodies (rod and cone), and beyond that the photoreceptor inner and outer segment layers.
Major neuronal cell classes. The 5 major neuronal cell classes in the retina are photoreceptors, bipolar cells, horizontal cells, amacrine cells, and ganglion cells. The main pathway through the retina is the sequence of photoreceptor to bipolar cell to ganglion cell. Horizontal cells modulate the signals from photoreceptors to bipolar cells, and amacrine cells modulate the output of bipolar cells to ganglion cells.
Müller cells. Müller cells are radially oriented glial cells that provide the initial scaffolding for retinal development and provide metabolic support for the neurons in the developed retina (see Figure 11–5).
Pigment epithelial cells. RPE cells not only reduce the scattering of unabsorbed photons, but are also important in nourishing the photoreceptor cells and in phagocytosis and recycling photopigment (see Figure 11–6).
PHOTORECEPTORS: ANATOMY, DISTRIBUTION, & FUNCTION
Anatomy of Rods and Cones
The first step in seeing is the capture of photons by photoreceptors. The 2 major types of photoreceptors, rods and cones, function in dim and bright light, respectively. Figure 11–8 shows a typical rod (left) and cone (right). A major structural difference between rods and cones is that, in rods, the photopigment is contained in disks that are completely internal to the outer segment of the receptors, whereas in cones, the cell membrane itself is folded into a comb-like membrane process that contains the photopigment. Rods and cones also differ in their distribution within the retina.
Rod and cone photoreceptors. The 2 major types of photoreceptors are the rod (left) and cone (right). Rods function in dim light, responding to <10 photons. Cones operate in bright daylight, requiring hundreds of photons per second. The rod photopigment is contained in disks that are completely internal to the outer segment of the receptors, whereas in cones, the photopigment lies in the cell membrane that is folded into a comb-like membrane process. Both rods and cones have 3 main structural elements: The outer segment contains the photon-absorbing photopigment in an array of disk-like membrane structures. The inner segment contains mitochondria and biochemical machinery for transporting the photopigment, such as rhodopsin, to the outer segment from its sites of synthesis in the cell body. Within the inner segment is the cell body that contains the nucleus and protein-manufacturing machinery. The synaptic terminal is where glutamate is released to regulate second-order cells (bipolar and horizontal cells).
Photoreceptors convert light into a modulation of the release of the neurotransmitter glutamate. This process is called phototransduction. Photoreceptors have 3 main structural parts, as illustrated in Figure 11–8:
The outer segment contains the photon-absorbing photo-pigment in an array of disk-like membrane structures. The plasma membrane of the outer segment has a high concentration of cyclic nucleotide–gated sodium/calcium channels.
The inner segment contains mitochondria and biochemical machinery for transporting the photopigment, such as rhodopsin, to the outer segment from its sites of synthesis in the cell body. Within the inner segment is the cell body that contains the nucleus and protein-manufacturing machinery.
The synaptic terminal is where glutamate is released to regulate second-order cells (bipolar and horizontal cells).
The outer segments of rods and cones interdigitate into the RPE, which provides essential metabolic support, such as resupplying new photopigment after it is bleached by light. The RPE also has a phagocytic function to degrade the distal tips of the rod and cone outer segments that are constantly being shed (see Figure 11–6). RPE dysfunction may cause photoreceptor death. This is a frequent cause of blindness, such as in RP.
Distribution of Rods & Cones
Unlike the imaging chip in a camera, which typically has a uniformly dense detector array, the retina has a much higher density of receptors in the center than in the periphery. Moreover, the mix of receptors also differs as a function of retinal location. Several aspects of the receptor density function are shown in Figure 11–9.
Distribution of photoreceptors in the retina. Cones are concentrated in the fovea and parafovea and then have a relatively constant distribution throughout the rest of the retina. Rods are absent from the fovea and parafovea, but peak in density just outside this region. Their density falls off more slowly toward the retinal periphery. The blind spot at the optic nerve head where the ganglion cell axons leave the eye has no cones or rods. (Reproduced with permission from Barrett KE, Barman SM, Brooks HL et al: Ganong’s Review of Medical Physiology, 26th ed. New York, NY: McGraw Hill; 2019.)
The horizontal axis of Figure 11–9 is eccentricity, in units of visual angle. What this refers to is the projection of the visual world onto the retina along a horizontal line that runs through the fovea and extends from the periphery of the retina closest to the nose (nasal retina) to the periphery closest to the cheek (temporal retina). The density of cones is strongly peaked within the central retina, which corresponds to just a few degrees of visual angle. This area is the fovea (see Figures 11–1 and 11–4), and the immediately surrounding region is the parafovea. Outside this region, the cone density is relatively constant out to the far periphery of the retina. Of the approximately 6.5 million cones in the retina, more than half are in the foveal region.
Not shown in this diagram is that fact that within the fovea center there are only green and red cones, but no blue cones. Blue cone density relative to green and red cones peaks slightly just outside the fovea in the parafovea, and then constitutes a relatively constant percentage of all cones throughout the rest of the retina, where the relative percentages are about 64% red, 32% green, and 2% blue. There are approximately 6.5 million cones in the human retina. Cones mediate daylight vision, including color.
The rod distribution is quite different from that of the cones. The fovea and parafoveal region are virtually rod free. Rod density peaks just outside this region, and then gradually declines out to the retinal periphery. Because rods mediate vision in dim light, it has long been known that in trying to locate a very dim object, such as a faint star, one should not look directly at the assumed location but just to the side of that location. Rods greatly outnumber cones across the retina except in the central foveal region. The retina contains approximately 120 million rods. The vertical density function follows a similar, but not identical, eccentricity profile for both rods and cones.
The blind spot is the retinal area where the ganglion cell axons become myelinated and exit the retina to form the optic nerve. There are no photoreceptors there. Generally, we are not aware of the blind spot for 2 reasons: (1) the blind spots in the 2 eyes are at different visual field locations; and (2) the brain “fills in” the lack of input based on surrounding neural activity. This also occurs during the slow onset of blindness; patients may lose considerable vision before they become consciously aware that there is any problem.
Rods mediate vision in dim light. The vast majority of mammals, including humans, have a single type of rod whose maximum sensitivity is to a wavelength of approximately 500 nm. Figure 11–9 shows that there are many more rods everywhere in the retina except the fovea, where they are completely absent. The human retina contains approximately 120 million rods. Rods are specialized to operate in very low light levels. Under ideal circumstances, a brief flash can usually be detected if approximately 5 to 7 rods each capture a single photon of light at about the same time. Individual rod cells are more sensitive to light because they express more photopigment and have higher amplification in the phototransduction cascade. Vision at low light levels mediated by rods is called scotopic vision.
Humans, like many primates, have 3 types of cones, called short-wavelength (blue), middle-wavelength (green), and long-wavelength (red) cones. When photoreceptors capture a photon of visible light, their response is the same regardless of its wavelength, because the molecular cascade that modulates glutamate release is the same regardless of the wavelength of the photon that is absorbed. This means that in dim light, where only rods are sensitive enough to generate visual signals, there is no color vision (vision is scotopic) because nothing about the wavelength of the absorbed photon is communicated to higher order retinal neurons. In bright light, however, retinal cells are sensitive to the ratio of activity of different cones, which varies with wavelength, and vision is photopic. Vision at high light levels mediated by cones is called photopic vision. Figure 11–10 shows the relative absorption efficiency for the short-, middle-, and long-wavelength cones (and rods) as a function of wavelength. Photons of any wavelength of light produce a unique ratio of activity of the 3 cones, allowing color to be identified independently of light intensity level. There is a regime at middle light levels in which both cones and rods operate to some extent. This is called mesopic vision.
Spectral sensitivities of human cones and rods. Human vision operates based on absorption of photons from just below 400 to nearly 700 nm. The 3 cone types and rods have different absorption curves. For the cones, the peaks are at 420, 534, and 564 nm for the blue, green, and red cones, respectively. Human rods have an absorption maximum at about 498 nm. The wavelength of the absorbed photon only affects its probability of absorption, not the receptor’s electrical response. Because of this, color vision depends on having multiple receptor types with different spectral sensitivity curves whose ratio of activity codes for wavelength. In dim light, only rods are active, so there is no color vision, but during the day, the 3 cones give us what is called trichromatic vision.
The Phototransduction Second Messenger Cascade
The absorption of a light photon by the photopigment in the photoreceptor outer segment (Figure 11–11A) initiates a cascade of intracellular events that leads to the modulation of glutamate release by the photoreceptors on to bipolar and horizontal cells. Key aspects of this cascade (described in the following text) are illustrated in Figure 11–11B:
The photopigment is formed by the protein opsin, which is bound to a molecule of retinal. Opsins are transmembrane proteins in the G-protein–coupled receptor family. When the photopigment molecule, such as rhodopsin in rods (or photopsins in cones), absorbs a photon, the retinal changes its stereoisomer form from the kinked structure called 11-cis retinal to a straighter form called all-trans retinal.
All-trans retinal separates from the protein opsin to which it was bound, allowing the opsin to be active.
The released opsin then activates transducin, a type of G protein. When activated, transducin dissociates its bound guanosine diphosphate (GDP) and binds to guanosine triphosphate (GTP).
The transducin-GTP complex activates phosphodiesterase, the enzyme that breaks down cyclic guanosine monophosphate (cGMP) into 5′-GMP. cGMP is a second messenger that promotes the opening of the cyclic nucleotide–gated (CNG) sodium/calcium channels in the outer segment of the photoreceptor. The reduction in the levels of cGMP reduces the number of open CNG channels (see Figure 11–11). Note that only sodium moving through this channel is depicted in Figure 11–11, but some other cations also transit this channel.
Closure of CNG channels causes hyperpolarization of the photoreceptor. Hyperpolarization is also contributed by the potassium current in the inner segment that pulls the membrane potential down toward the equilibrium potential for potassium (EK). The sodium-potassium transporter pump works to counteract the effect of the dark current and maintain the normal cell low sodium–high potassium concentration gradients.
The hyperpolarization of the photoreceptor causes its synaptic terminal (see Figure 11–8; also called the pedicle) to release less glutamate, the photoreceptor neurotransmitter.
The modulation of glutamate release drives other cells in the retina. Specifically, the outputs of photoreceptors drive 2 main types of cells, called bipolar and horizontal cells.
Phototransduction. A. The photopigment molecules reside in internal disks in rods but in the cell membrane in cones. In rods, as shown, the photopigment is formed by the protein opsin, bound to a molecule of retinal. B. When the photopigment molecule absorbs a photon, the retinal unit changes its stereoisomer form from the kinked structure called 11-cis retinal to a straighter form called all-trans retinal. All-trans retinal separates from the protein opsin to which it was bound, allowing the opsin to be active. The released opsin then activates transducin, a type of G protein, which dissociates its bound guanosine diphosphate (GDP) and binds to guanosine triphosphate (GTP). The transducin-GTP complex activates phosphodiesterase (PDE), the enzyme that breaks down cyclic guanosine monophosphate (cGMP) into 5′-GMP. cGMP is a second messenger that promotes the opening of the cyclic nucleotide–gated (CNG) sodium/calcium channels in the outer segment of the photoreceptor. The reduction in the levels of cGMP reduces the number of open CNG channels, which flux sodium primarily, depolarizing the cell when open, but closure of CNG channels causes hyperpolarization of the photoreceptor. The hyperpolarization of the photoreceptor causes its synaptic terminal to release less glutamate, the photoreceptor neurotransmitter. The modulation of glutamate release drives bipolar and horizontal cells. (Part A, reproduced with permission from Mescher AL. Junqueira’s Basic Histology: Text & Atlas, 15th ed. New York, NY: McGraw Hill; 2018; part B, reproduced with permission from Zhang X, Cote RH. cGMP signaling in vertebrate retinal photoreceptor cells, Front Biosci. 2005 May 1;10:1191-1204.)
Dark Currents & Synaptic Glutamate Release
cGMP concentrations in photoreceptor outer segments are high in the dark, and this ensures that the percentage of open CNG sodium/calcium channels is high. A large number of potassium channels are continuously open in the inner segment. Thus, in the dark, the simultaneous entry of sodium and calcium in the outer segment and exit of potassium in the inner segment produce the dark current. The dark current holds the membrane potential at about –40 mV, so glutamate release is high in the dark. Closure of the outer-segment CNG sodium/calcium channels by the light, from reduction of cGMP concentration, allows the excess potassium current in the inner segment to hyperpolarize the photoreceptor to approximately –60 mV. This hyperpolarization reduces the release of glutamate from the photoreceptor terminal. Hyperpolarization in response to light occurs in the photoreceptors of all vertebrates. However, many invertebrates operate in an opposite mode and have photoreceptors that depolarize to light via photochemical mechanisms.
The visual system has evolved to function from light levels at which single rods absorb a few photons per second, to levels where cones absorb millions. This dynamic range is mediated by 3 types of adaptation: (1) the use of rods in dim light and cones in bright light; (2) light and dark adaptation by rods and cones themselves within their operating range; and (3) adaptation by other retinal neurons. Cones function in light levels from daylight shadows to reflection off snow, which constitutes a range of about 8 log units of light intensity. Rods adapt over a range from a few photons per second to hundreds, or about 2 log units of background intensity. Adaptation allows the photoreceptors to generate relatively large signals for small changes in light level or the mean illumination at that time of day. Adaptation involves processes within photoreceptors and within the retinal circuitry. Schematically, regardless of the locus, adaptation depends on detecting the mean light level and dividing or subtracting that level from the direct response to light intensity, as illustrated in Figure 11–12.
Sensory adaptation. Adaptation involves changing the response range of a retinal neuron, such as a bipolar cell, depending on the mean light level. If the stimulus versus response function spanned the entire stimulus range, as on the left, the response difference for typical light excursions about any mean level would be quite small. On the other hand, having a highly sloped response versus stimulus function, as on the right, leads to saturation at higher light levels. The solution is to shift the highly sloped function so that it is always centered at the average light level. This is done by a divisive or subtractive process that estimates the mean light level and moves the function to that level. At the photoreceptor to bipolar cell synapse this is done by horizontal cells that summate input from neighboring photoreceptors and, via inhibition, reduce the photoreceptor to bipolar cell drive in a proportional manner to shift the bipolar response operating curve to be centered at the current overall light level.
One important place this is done is at the photoreceptor to bipolar cell synapse, mediated by horizontal cells. Horizontal cells summate input from neighboring photoreceptors and, via inhibition, reduce the photoreceptor to bipolar cell drive in a proportional manner. The result is a shift of the operating curve of the bipolar cell, so that its response range is adjusted to be centered at the current overall light level (illustrated in Figure 11–12).
Most blindness in the developed world is caused by photoreceptor degeneration (the major exception is glaucoma, in which retinal ganglion cells degenerate). Photoreceptors are highly specialized cells with intense metabolic and protein trafficking demands placed on them by the processing of visual pigments. Photoreceptors also depend on metabolic support by the pigment epithelium, into which their outer segments interdigitate, so that pigment epithelium dysfunction can secondarily produce photoreceptor degeneration.
Macular degeneration. Macular degeneration refers to a loss of vision in the center of the visual field (the macula) because of damage to the photoreceptors in this central region of the retina. It can be differentiated into so-called “dry” and “wet” types. Dry macular degeneration (often called age-related macular degeneration) is associated with the accumulation of drusen (a kind of cellular debris) that accumulates between the choroid (blood vessel network distal to the pigment epithelium that nourishes the retina) and the retina (see Figures 11–4 and 11–5). Death of photoreceptors mediating central vision occurs. Dry age-related macular degeneration is more prevalent in the elderly and typically has a slow progression. Its progression can sometimes be slowed with dietary modification.
Wet macular degeneration occurs when blood vessels sprout (neovascularization) from the choroid behind the retina. These neovascular vessels often leak, leading to retinal scarring and cell death. The retina can also become detached, with the detached portion also dying. It is sometimes treated with laser photocoagulation therapy to limit neovascularization.
Retinitis pigmentosa. Retinitis pigmentosa is a progressive degenerative, inherited pathology caused either by genetic defects in the rod photoreceptors or the RPE. It typically begins with loss of night vision due to rod death and progresses to tunnel vision from death of all peripheral photoreceptors. Ultimately, total blindness can occur. Mutations in >35 genes have been linked to RP, with mutation in the rhodopsin gene responsible for approximately 25% autosomal dominant RP.
Color blindness and anomalies. Color vision is possible when there are different receptor types with different spectral sensitivities, which is the probability of absorbing light as a function of the wavelength (see Figure 11–10). Humans with normal color vision are called trichromats because they have 3 distinct cone types. However, most mammals and many partially colorblind humans have only 2 cone types and are called dichromats. Dichromacy is usually caused by a pigment allele mutation in which either the green cone is switched to a red pigment (deuteranope) or the red cone is switched to green (protanope), so that the dichromat has about the normal number of cones but no red-green opponency. It is also possible to lose the blue cone system altogether, although that is rarer (tritanope). Calling humans who are missing a cone type “colorblind” is a misnomer because these people are color deficient in only part of the spectrum. Colorblindness is an X-linked recessive disorder. The genes for the red and green cones are located on the X chromosome. Because women have 2 X copies, they need 2 defective genes to have this colorblindness. But because men have only 1 X chromosome, 1 mutation gives the defect to a man. Red-green color blindness occurs in approximately 5% of men, but only 0.25% of women. Tritanopes who are missing a blue cone do not see well at all in the blue end of the spectrum because they lack the blue cone that is sensitive there. Some hereditary conditions and retinal degenerations, such as RP, result in retinas with no rods. These people are night blind. Anomalous (abnormal) color vision occurs when a person has cones with a different spectral sensitivity than a “normal” person. This produces poorer color vision in most cases, but some cases result in better color vision. For example, because a woman has 2 X chromosomes, if she has 2 different genes for the same cone but with different spectral sensitivities, she can be effectively a tetrachromat (4 colors).
RETINAL VISUAL PROCESSING: RETINAL CIRCUITS
The end effect of the absorption of photons by photoreceptors, which communicate via graded potentials, is the modulation of the release of glutamate at the photoreceptor synaptic terminal. This modulated glutamate release activates the network of neurons in the retina that culminates in the firing of action potentials by retinal ganglion cells, whose axons form the optic nerve and project to several retinal recipient zones in the brain, most notably the lateral geniculate nucleus of the thalamus and the superior colliculus.
Photoreceptor Synaptic Release
The glutamate release from photoreceptor synaptic terminals occurs at what is called a ribbon synapse. This synapse, which involves robust release of glutamate due to its morphology, is common in the retina but rare elsewhere in the CNS. The postsynaptic receptors for glutamate released by the photoreceptors are found on the dendrites of 2 major classes of cells—bipolar and horizontal cells—with the synapses located in the outer plexiform layer (see Figure 11–7). Bipolar cells transmit the photoreceptor signal from the outer plexiform layer to the inner plexiform layer, where they synapse onto the dendrites of amacrine and ganglion cells. Horizontal cell processes modify the photoreceptor to bipolar cell message in a lateral inhibitory network.
Bipolar & Horizontal Cells
Horizontal Cells & Lateral Inhibition
Horizontal cells receive inputs from multiple photoreceptor cells and synapse back onto those photoreceptors. Their role in retinal signal processing is to modulate the signal from photoreceptor to bipolar cells via lateral inhibition. Horizontal cells are activated by photoreceptors over a large region. This produces an estimate of the average local light intensity, a percentage of which is then subtracted from the output of the central photoreceptor that activates a particular bipolar cell. Thus, horizontal cells cause photoreceptors to communicate to bipolar cells the difference between the light they receive and the surrounding light. This is called local contrast, which is relatively independent of overall luminance level (see Figure 11–12). Horizontal cells contact only photoreceptors and other horizontal cells and do not send outputs to ganglion or amacrine cells.
Because photoreceptors are hyperpolarized by light and inhibited by horizontal cells activated by surrounding photoreceptors, more glutamate is released for areas of the image that are darker than the local average, and less glutamate is released for areas brighter than the local average. At all but the lowest light levels, objects are represented by a small modulation around the ambient light level that is either above or below that level. Object detection based on detecting this modulation is robust and independent of the ambient light level. Horizontal cell lateral inhibition reduces redundancy in retinal signals. Thus, the bipolar cell signals the difference between the activation it receives from photoreceptors connected directly to it and the surrounding average intensity.
Different bipolar cell types receive synaptic input from either rods or cones and are distinguished as rod or cone bipolar cells. Cone photoreceptors can synapse onto bipolar cells having 2 different types of response, hyperpolarizing or depolarizing, thus splitting the photoreceptor signal at the first synapse in the retina between depolarizing (on) and hyperpolarizing (off) pathways. This is accomplished by the presence of 2 main types of bipolar cells, which are called depolarizing (on) and hyperpolarizing (off), depicted in Figure 11–13. Hyperpolarizing (off) bipolar cells express AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid)/kainite–type receptors for glutamate and depolarize when their photoreceptors do, in the dark, and hyperpolarize in response to light. Depolarizing (on) bipolar cells have an inhibitory receptor for glutamate (metabotropic MGluR6) that inverts the signal from photoreceptors so that these bipolar cells hyperpolarize to dark and depolarize to light. In summary, in the dark, a photoreceptor cell releases glutamate, which hyperpolarizes (and inhibits) “on” bipolar cells and depolarizes (excites) “off” bipolar cells. In the light, photoreceptor cells release less glutamate; this causes the on bipolar cell to lose its inhibition and become active (depolarized), whereas the off bipolar cell loses its excitation (becomes hyperpolarized) and becomes silent. Similar to the photoreceptors, bipolar cells also use glutamate and graded responses to communicate to their targets, amacrine cells and retinal ganglion cells. (In Figure 11–13, the bipolar cells are referred to as on-center and off-center.) Most mammalian retinas actually have about 10 distinct types of bipolar cells. These include a depolarizing and hyperpolarizing bipolar cell type for each of the 2 or 3 cone types and at least 1 bipolar cell type that receives inputs from rods. Bipolar cells also vary regarding whether they receive input from either a large or small number of photoreceptors.
Depolarizing and hyperpolarizing bipolar cells transmit high and low local contrast in 2 parallel pathways. On the left, when the light level is high, the photoreceptors are hyperpolarized and release less glutamate. This reduces the inhibitory input to depolarizing bipolar cells, whose MGluR6 receptors are potassium selective, and they depolarize. These bipolar cells typically make excitatory synapses onto the dendrites of on-center ganglion cells, exciting them for light increases. On the other hand, hyperpolarizing bipolar cells have AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid)/kainite excitatory receptors for glutamate, so they hyperpolarize to light when the photoreceptors do the same, as do the off-center ganglion cells. At light offset, on the right, the photoreceptors are depolarized, inhibiting depolarizing bipolar cells and on-center ganglion cells, but exciting hyperpolarizing bipolar cells and off-center ganglion cells.
The bipolar cell situation is different for rods compared to cones. Rods connect only to depolarizing rod bipolar cells. These bipolar cells make gap junction contacts with depolarizing cone bipolar cells and thus activate on-center ganglion cells (and amacrine cells) through the depolarizing cone bipolar cell terminals. The depolarizing rod bipolar cells also have inhibitory, glycine-mediated outputs to hyperpolarizing cone bipolar cells. By disinhibiting these cells for light increases, they activate them for light decrements.
The 2 major bipolar cell types establish 2 parallel pathways in the retina that respond to stimuli lighter than the background (on bipolar cells) or darker than the background (off bipolar cells). Bipolar cell terminals connect to the dendrites of 2 kinds of postsynaptic cells: amacrine and ganglion cells.
Bipolar Cell Inputs to the Inner Plexiform Layer
Bipolar output synaptic terminals end in separate layers of the inner plexiform layer, with depolarizing on bipolar cells terminating in the proximal part of the inner plexiform layer and hyperpolarizing off bipolar cells terminating in the distal inner plexiform layer. These parallel on and off pathways are maintained through the connections to the retinal ganglion cells and to the thalamus.
Laterally Inhibitory Amacrine Cells
Amacrine cells are laterally interacting interneurons. Some have a similar function in the inner plexiform layer to that of horizontal cells in the outer plexiform layer. These amacrine cells conduct inhibitory signals from the surrounding bipolar cells, so that the ganglion cell responds to the difference between the light in its central area and the surrounding area. This action reduces the amount of redundant information that ganglion cells must transmit.
Amacrine Cells Generate Complex Receptive Field Properties
Some amacrine cells generate complex receptive field properties. Other amacrine cells sculpt the bipolar cell output to ganglion cells to produce a variety of ganglion cell classes that respond to particular features of the visual input, such as motion, edges, or colors. Most amacrine cells use the neurotransmitter γ-aminobutyric acid (GABA), but others use glycine, neuropeptides, and even acetylcholine to produce complex ganglion cell response properties. Thus, from a limited number of bipolar cell types, there emerge ganglion cell classes that respond to different colors, movement, or the presence of long edges or corners. Over 30 classes of amacrine cells help to create all these ganglion cell classes.
Retinal ganglion cells are the sole output from the retina. Their axons form the optic nerve that conducts action potentials to approximately 15 retinal recipient zones in the brain. The most important of these for visual acuity and perception is the projection to the lateral geniculate nucleus (LGN) of the thalamus. Important projections are also made to the hypothalamus and midbrain areas such as the pretectal and accessory optic system nuclei.
Thalamic Layer-Projecting Ganglion Cell Classes
On and off bipolar cells are connected to similarly responding ganglion cells called on-center and off-center ganglion cells, respectively (Figure 11–14). The 2 major ganglion cell classes project to distinct layers within the dorsal LGN of the thalamus. These ganglion cell classes are called parvocellular (which means small) and magnocellular cells, although they may also be called midget and parasol cells, respectively. Both parvo- and magnocellular ganglion cells have so-called “concentric” receptive fields. Concentric means that there is an excitatory central region, usually coextensive with the ganglion cell dendritic tree, in which light-on stimulation produces an excitatory response in on-center ganglion cells, whereas light-off stimulation produces and excitatory response in off-center ganglion cells. Usually the best response occurs when the light increment or decrement exactly matches or fills the excitatory receptive field center region.
Ganglion cell receptive field sensitivity. Most ganglion cells that project to the thalamus have “concentric” receptive fields. This means that the optimal stimulus just fills what is called the excitatory receptive field center, with spots smaller or larger producing weaker responses. The surrounds of concentric ganglion cells are also antagonistic, which means that light offset is excitatory in the surround of on-center ganglion cells (bottom left), whereas light onset is excitatory in the surround of off-center ganglion cells (bottom right).
Concentric receptive field ganglion cells have regions surrounding the excitatory center that have the following 2 main characteristics. (1) Stimulation with spots larger than the receptive field center, that is, invading the inhibitory surround, produces a weaker response than stimulation confined to the center; hence the name, inhibitory surround. (2) The surround also has a property called “antagonistic.” An antagonistic surround is one in which surround stimulation in an on-center ganglion cell produces light-offset excitation, whereas light-onset stimulation produces an excitatory response in off-center ganglion cells (see bottom of Figure 11–14). Both parvo- and magnocellular ganglion cells that form the main projection to the LGN of the thalamus have antagonistic surrounds, but many other ganglion cells have only inhibitory surrounds.
Parvocellular/Midget Ganglion Cells
In the fovea, all ganglion cells are a particular type of parvocellular ganglion cell in a neural circuit called the midget system, in which a single photoreceptor (a cone) activates a single bipolar cell, which feeds a single ganglion cell. However, outside the fovea, there are generally many photoreceptors (rods or cones) that are connected to 1 bipolar cell and several bipolar cells are input to 1 parvocellular ganglion cell. The responses of parvocellular ganglion cells resemble their respective depolarizing or hyperpolarizing bipolar cell input, except that the ganglion cell excitatory postsynaptic potential produces action potentials that will transmit the ganglion cell message via its axons to the brain. Parvocellular ganglion cells have brisk-sustained responses, meaning that they have high action potential firing rates that are well modulated by small changes in light intensity. These are the most numerous ganglion cells in the human retina, constituting approximately 1 million of the approximately 1.2 million total ganglion cells. They form the main projection to the upper 4 layers of the LGN of the thalamus, called the parvocellular layers, which is a relay in the high-acuity, conscious visual pathway. Parvocellular ganglion cells code for color and fine detail. Their small size and small receptive fields mediate very high acuity in the human fovea.
Magnocellular/Parasol Ganglion Cells
Virtually all mammalian retinas also have the magnocellular ganglion cell class. Although absent from the fovea itself, these ganglion cells range from just outside the immediate fovea to the extreme periphery. Magnocellular ganglion cells respond more transiently than parvocellular cells, and they have larger integration areas (receptive fields) than parvocellular cells at any given eccentricity. Magnocellular ganglion cells have relatively more amacrine inputs than parvocellular ganglion cells and respond well to changes in the visual image, such as motion, even at low contrast. They project to the bottom 2 layers of the LGN of the thalamus, the magnocellular layers, in primates.
Other Ganglion Cell Classes
The network of amacrine cells also gives rise to ganglion cell classes that respond only to specific features of the visual input. Some of these ganglion cell classes project to the thalamus, but others project to different brain areas. Bistratified retinal ganglion cells project to the koniocellular layers of the LGN and are proposed to function in color vision. Directionally selective ganglion cells are not only sensitive to movement, but also to its direction. These cells project to a variety of brain nuclei that enable target tracking and using vision to maintain balance and orientation. A small percentage of ganglion cells are intrinsically light sensitive. This means that they express their own photopigment that causes them to respond directly to light, without photoreceptor input. These intrinsically photoreceptive ganglion cells are sensitive to the overall light level, and they project to the suprachiasmatic nucleus in the hypothalamus and control circadian rhythms. Other intrinsically photoreceptive ganglion cells project to the Edinger-Westphal nucleus and control the pupillary light reflex.
The visual system is thought to interpret color in an antagonistic way, with antagonism occurring at the level of ganglion cells. A range of wavelengths stimulate each of the cone types to varying degrees. Color vision requires that the signals from different cone types be kept separate until color-opponent ganglion cells can compare the ratio of activity between cones. The activity of red cones is typically opposed to the activity of green cones in some color-opponent ganglion cells. The other main type of color-opponent ganglion cell has blue opposed to the combination of red and green. Color opponency is another parallel visual pathway, like on versus off in the bipolar and ganglion cells.
The major disease of ganglion cells is glaucoma, one of the leading causes of blindness. Glaucoma is an optic neuropathy associated with elevated intraocular pressure in the aqueous humor, in which retinal ganglion cells die due to damage to their axons. However, glaucoma causing optic nerve damage can also occur in individuals with normal intraocular pressure. Retinal ganglion cells tend to be lost in a characteristic pattern with an associated expanding visual field loss that often progresses to blindness. There are 2 main categories of glaucoma: open-angle and closed-angle. Open-angle glaucoma is chronic, typically symptomless, and of slow progression until significant vision has been lost. It is associated with poor drainage of the scleral venous sinus that builds up pressure in the anterior chamber and then the vitreous.
Closed-angle glaucoma refers to the situation where the iris sticks to the lens, preventing fluid from escaping from the vitreous to the anterior chamber. It often has a sudden painful onset. Treatment can involve using a laser to make a hole in in the iris to allow drainage, but without treatment, vision can rapidly deteriorate.
In both types of glaucoma, ganglion cell axons in the periphery tend to die first so that visual field loss tends to progress from the periphery to the center, yielding a stage near the end of the disease characterized as “tunnel vision.”
What Does the Human Eye Tell the Human Brain?
Although the exact number of distinct ganglion cell classes in the human eye is unknown, the number is likely to be at least 20, as is the case with other mammals in which this issue has been investigated. How are these ganglion cell classes distributed across the retina? Like the photoreceptors, ganglion cells show an eccentricity factor: Ganglion cell somas and dendritic trees are smaller in and near the fovea than in the periphery. At each locus (eccentricity) in the retina, each ganglion cell class appears to tile the retina, with no gaps between dendritic trees and little overlap. However, the size of each ganglion cell class at each eccentricity varies as a function of class.
Figure 11–15 illustrates how, at 1 particular retinal location, 6 to 7 parvocellular ganglion cells might tile the interior of 1 magnocellular ganglion cell. The magnocellular ganglion cells themselves form a similar tiling on a larger scale. If there are 20 ganglion cell classes and each tiles the retina, then every point on the retina is within the receptive field of 1 of each of the 20 different ganglion cell classes, each of which extracts some particular information from the visual scene for projection to the brain (where there are at least 15 different retinal recipient zones). Some of these ganglion cells care about color, others about edges, and still others about movement. The retina does not transmit a picture of the visual scene for the brain to analyze; rather, it transmits 20 transforms of the visual scene that are used by the brain for perception and visually guided behavior in many different ways. This must be clear from the numbers: There are >120 million photoreceptors but only approximately 1.2 million ganglion cells. Only in the midget/parvocellular system within the fovea does the retina approach the idea of sending the output of a single cone via a single ganglion cell to the brain. Elsewhere, each parvocellular ganglion cell extracts some average chromatic signal from the photoreceptors that influence it, and other ganglion cells extract more complex information.
Tiling by parvocellular ganglion cells within the receptive field of a magnocellular cell. At any given retinal location, 6 to 7 parvocellular ganglion cells might tile the interior of 1 magnocellular ganglion cell. The magnocellular ganglion cells themselves form a similar tiling on a larger scale. The more numerous parvocellular ganglion cells with smaller receptive fields constitute the highest acuity visual pathway for perceptual acuity. These cells may also be more important in color vision than magnocellular ganglion cells.
Vision is a hierarchical process.
Mechanical elements of the eye, such as the lens and pupil, control the focus and intensity of light reaching the retina.
Eye movements are an integral part of visual processing.
Retinal photoreceptors convert captured photons to modulated glutamate release.
Retinal bipolar cells communicate positive and negative excursions around the mean light level to the inner retina.
Amacrine and ganglion cells in the inner retina sculpt and transmit extracted aspects of the changing light distribution for transmission to the brain.
Retinal ganglion cells project to 15 different retinal recipient zones in the brain.
The most important retinal recipient zone is the lateral geniculate nucleus of the thalamus.
Blindness and visual deficits occur primarily in the retina, but also in higher visual processing centers.