Visual System Anatomy

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The visual system includes the eyes, connecting pathways through to the visual cortex, and other parts of the brain (see the image below). The neural signals initially processed by the retina travel via the axons of the ganglion cells through the optic nerves, dividing and partially crossing over into the optic chiasm and then travelling via the optic tracts to the lateral geniculate nucleus (LGN). From the LGN, the signals continue to the primary visual cortex, where further visual processing takes place.

The eye has many features of a camera, beginning with the cornea and ending with the occipital (visual) cortex. The cornea, the anteriormost structure of the globe, is a dome-shaped translucent tissue that functions to bend (refract) light rays. These light rays pass through the anterior and posterior segments of the eye and are focused onto the retina by the action of the lens. The image focused on the retina is inverted from top to bottom and reversed from right to left. ^{[1, 2, 3, 4]}

Visual processing and, ultimately, visual fields begin in the retina. Light enters the eye; passes through the cornea, anterior chamber, lens, and vitreous; and finally reaches the photoreceptor cells of the retina. Light activates these photoreceptors, which modulate the activity of bipolar cells. The bipolar cells synapse with the ganglion cells. The axons of the ganglion cells form the optic nerve, which carries information to the brain.

The receptor cells and the bipolar cells of the retina respond to light with graded electrotonic responses, rather than with all-or-nothing action potentials. The graded responses in the photoreceptors are the result of the photochemical process, but those in the bipolar cells are synaptically driven. Furthermore, the photoreceptors respond to light with a hyperpolarizing receptor potential that is accompanied by an increase in membrane resistance to Na⁺ influx.

In the absence of light (ie, dark adaptation), a constant influx of Na⁺ ions (dark current) occurs through the outer segment membrane of photoreceptors, giving rise to a resting membrane potential of about -40 mV. The continuous influx of sodium ions results from binding of cyclic guanosine monophosphate (cGMP) to the sodium gates, which keeps the gated channels open while maintaining neurotransmitter release onto the bipolar cell, hyperpolarizing it (ie, the bipolar cells are inhibited).

Both rods and cones release L-glutamate at their terminals on bipolar cells. In “off” bipolar cells, L-glutamate activates the KA/AMPA receptor to produce hyperpolarization. In “on” bipolar cells, L-glutamate activates L-AP4 receptors to produce depolarization.

A light flash decreases the dark current and hyperpolarizes the photoreceptors relative to the dark state, reducing the amount of inhibitory neurotransmitters released onto the bipolar cell. In light adaptation, rhodopsin is activated (ie, 11-cis -retinal is photoisomerized), and the attached G-protein (transducin) is also activated. The activated G-protein activates cGMP phosphodiesterase, which catalyzes the conversion of cGMP to guanosine monophosphate (GMP).

The conversion of cGMP to GMP closes sodium channels. Sodium influx ceases, resulting in hyperpolarization of the photoreceptor cells. This hyperpolarization decreases the release of glutamate. The bipolar cells, no longer inhibited, release neurotransmitters, which stimulate the ganglion cells to generate action potentials.

The primary line of information transmission is from photoreceptor to bipolar cell to ganglion cell and then to the brain, but the amacrine and horizontal cells provide lateral transmission lines that can produce the complicated center-surround receptive fields of ganglion cells. Like the bipolar cells, the horizontal cells receive their inputs from receptors, and they generate no spikes.

Horizontal cell outputs inhibit (ie, reduce transmission at) nearby unilluminated receptor-bipolar cell synaptic junctions. Some have suggested that these outputs may enhance contrast by strongly turning off unstimulated bipolar cells. Amacrine cells produce action potentials and enter into reciprocal synaptic relations with bipolar cells. The horizontal cells and the amacrine cells are responsible for lateral interactions within the retina.

The bipolar cells and ganglion cells are organized in such a way that each cell responds to a small circular patch of photoreceptors, which defines the cell’s receptive field. The receptive fields of retinal ganglion cells are concentric, consisting of a roughly circular central area and a surrounding ring. Ganglion cells have 2 basic types of receptive fields: on-center/off-surround and off-center/on-surround. The center and its surround are always antagonistic and tend to cancel out each other’s activity.

When light hits the surround region of an on-center ganglion cell, the level of activity in the cell decreases; conversely, when light hits the center of the receptive field, the cell’s activity increases. In these cells, a maximal response is achieved when light illuminates the entire center of the receptive field. If light only illuminates the surround region, the ganglion cell is maximally inhibited. If both the center and the surround region are illuminated, the response is just above baseline (with center effects slightly stronger than surround effects).

When light enters the surround region of an off-center ganglion cell, the level of activity in the cell increases; when light enters the center of the receptive field, cellular activity decreases. Light illuminating the entire center of an off-center ganglion cell results in cellular inhibition, and a maximal response is achieved when light illuminates the entire surround region. As with an on-center ganglion cell, when both the center and the surround region are illuminated, the response changes little from baseline.

Thus, uniform illumination of the entire receptive field is less effective in activating a ganglion cell than is a well-placed small spot or a line or edge that passes through the center of the cell’s receptive field. This organization makes the ganglion cells sensitive to differences in the level of illumination across the receptive field—that is, what is termed luminance contrast.

Luminance contrast is dependent on the position of the receptive field. By combining information from adjacent receptive fields, the brain can construct information about edges and, ultimately, shapes. In short, cells whose activity is most affected have receptive fields whose center is adjacent to the light-dark edge. Therefore, the information supplied by the ganglion cells to the brain does not give equal weight to all parts of the visual scene; rather, it emphasizes features that convey the most important information (eg, boundaries and edges).

The field of vision the 2 eyes can see in primary gaze is termed the visual field. Each eye sees only a segment of this visual field. The visual field can be divided into the right and left hemifields. The temporal left retina and the nasal right retina are responsible for the right hemifield, whereas the nasal left retina and the temporal right retina are responsible for the left hemifield.

The right and left hemifields overlap extensively in the central portion, giving rise to the binocular field of vision. Vision in the periphery (ie, outside the binocular field of vision) is strictly monocular, mediated primarily by the most medial portion of the nasal retina.

The center of the visual field projects its image onto the fovea of the retina. The fovea is a region on the retina where cones are most concentrated. This anatomic arrangement, along with the 1-to-1 relation between the cones and the bipolar and ganglion cells, explains why visual acuity is highest in this region.

The axons of the ganglion cells exit the eye at the level of the lamina cribrosa, collectively forming the optic nerve. Each optic nerve consists of approximately 1 million retinal ganglion cell axons. The nerve connects to the posterior aspect of the eye in a position that is about 15° nasal to the macula. The optic nerve head is approximately 1.8 mm (0.07 in.) in diameter.

The area where the axons exit the eye is called the optic disc. Because no receptors exist in this region, nothing can be seen in the corresponding part of the visual field. This blind spot appears not as a dark spot (ie, scotoma) but simply as a region from which one cannot obtain visual information. The blind spot is approximately 5° in size and about 15° temporal to fixation in the visual field of each eye. When both eyes are open, the blind spot of each eye is filled in by the visual field of the other eye.

The optic nerves of the 2 eyes continue posteriorly and meet at the optic chiasm, located just anterior to the stalk of the pituitary gland. At the optic chiasm, the optic nerves decussate. The axons from the nasal retina cross over to the opposite (ie, contralateral) side of the brain, and the axons from the temporal retina project ipsilaterally.

After the axons of the ganglion cells pass the optic chiasm, they are collectively referred to as the optic tract. Posterior to the optic chiasm, the information carried from the left visual field is carried in the right optic tract, whereas the information from the right visual field is carried in the left optic tract. Each optic tract terminates at the lateral geniculate nucleus (LGN), which is the visual part of the dorsal thalamus.

The vast majority of the axons of the right and left optic tracts terminate in the right and left LGNs. The LGN serves as the primary relay nucleus for visual processing by the cerebral cortex. The right LGN receives information from the left visual field via the right optic tract, and the left LGN receives information from the right visual field via the left optic tract (see the image below). It is here that visual information to the brain—specifically, the visual cortex—appears to be regulated and the first stage of coordinating vision from the 2 eyes begins.

Each LGN has 6 layers: 3 that receive input from the right eye, and 3 that receive input from the left eye. Because of the way in which the retinal ganglion cell axons are distributed through the chiasm and on to the optic tracts, the information processed in any single layer of the LGN represents specific areas of the visual field for 1 eye. The spatial relationships among the ganglion cells in the retina are maintained in their targets as orderly representations or “maps” of visual space.

Four of the layers of the LGN are composed of the parvocellular (small) ganglion cells from the retina, which come primarily from the fovea. These cells are most sensitive to color and fine detail. Two of the layers are composed of the magnocellular (large) ganglion cells from the retina. These cells are mostly from the perifoveal and more peripheral areas of retina and are largely responsible for the processing of motion. From the LGN, visual information is relayed to the visual cortex.

Some of the axons in the tract project to the superior colliculi, paired structures located on the roof of the midbrain. The superior colliculi help coordinate rapid movements of the eye toward a target. Axons from the optic tract also project to the suprachiasmatic nucleus (SCN) in the hypothalamus. Cells in the SCN are involved in the control of circadian rhythms related to the light-dark cycle.

Finally, axons of ganglion cells project to the pretectum, a region located between the thalamus and the midbrain. The pretectum serves an important function as the coordinating center for the pupillary light reflex.

Most of the axons form LGN neurons from the optic radiations, which terminate in the visual areas in the occipital cortex. Fibers in the optic radiation that carry information about the superior visual field sweep around the lateral horn of the ventricle in the temporal lobe before reaching the occipital cortex. The superior fibers of the optic radiation are commonly known as Meyer’s loop. Fibers in the optic radiation that carry information about the inferior visual field travel in the parietal lobe.

The topographic order of visual information and the final processing of the neural signals from the retina are maintained in the visual cortex. The fovea is represented in the posterior part of the visual cortex, and the more peripheral regions of the retina are represented in progressively more anterior regions. Note that the area of central vision (ie, the fovea) is represented over an especially large part of the visual cortex. Inputs from the 2 eyes converge at the cortical level, making binocular vision possible.

A total of 6 separate areas in the visual cortex exist: V1, V2, V3, V3a, V4, and V5. The primary visual cortex, or V1, is the first structure in the visual cortex, where the neurons form the LGN synapse. In V1, the neural signals are interpreted in terms of visual space, including the form, color, and orientation of objects. V1 dedicates most of its area to the interpretation of information from the fovea. This mapping is known as cortical magnification and is typical in primates and animals that rely on information from the fovea for survival.

From V1, the signals pass through to V2, where color perception occurs and form is further interpreted. As the neural signals continue further into other areas of the visual cortex, more associative processes take place. The primary visual cortex (V1, or striate cortex) projects to other areas of the cerebral cortex (extrastriate cortex) that are involved in complex visual perception.

In the portions of the visual cortex that make up the parietal visual cortical areas, motion of objects, motion of self through the world, and spatial reasoning are processed. In the temporal visual cortical areas, including the middle temporal area (V5), recognition of objects through interpretation of complex forms takes place (high-resolution form vision, object recognition, and pattern recognition).

The final psychological and perceptual experience of vision also includes aspects of memory, expectation, prediction, and interpolation that are subserved by other apparently nonvisual areas of the brain.

American Academy of Ophthalmology. Section 5: Neuro-Ophthalmology. 2011-2012 Basic and Clinical Science Course. 2011.

Purves D. Neuroscience. 4th ed. Sunderland, CT: Sinauer Associates; 2008.

Haines DE. Fundamental Neuroscience for Basic and Clinical Applications. 3rd ed. St Louis: Mosby-Elsevier; 2008.

Patton KT, Thibodeau GA. Anatomy & Physiology. 7th ed. St Louis: Mosby-Elsevier; 2010.

Hon-Vu Q Duong, MD Clinical Instructor of Ophthalmology and Ophthalmic Pathology, Westfield Eye Center; Senior Lecturer of Neurosciences:Anatomy and Physiology, Nevada State College

Hon-Vu Q Duong, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Thomas R Gest, PhD Professor of Anatomy, Department of Medical Education, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Disclosure: Nothing to disclose.

Visual System Anatomy

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