Physiology 5th Ed.

VISION

The visual system detects and interprets light stimuli, which are electromagnetic waves. The eye can distinguish two qualities of light: its brightness and its wavelength. For humans, the wavelengths between 400 and 750 nanometers are called visible light.

Structures of the Eye

The major structures of the eye are illustrated in Figure 3-12. The wall of the eye consists of three concentric layers: an outer layer, a middle layer, and an inner layer. The outer layer, which is fibrous, includes the cornea, corneal epithelium, conjunctiva, and sclera. The middle layer, which is vascular, includes the iris and the choroid. The inner layer, which is neural, contains the retina. The functional portions of the retina cover the entire posterior eye, with the exception of the blind spot, which is the optic disc (head of the optic nerve). Visual acuity is highest at a central point of the retina, called the macula; light is focused at a depression in the macula, called the fovea. The eye also contains a lens, which focuses light; pigments, which absorb light and reduce scatter; and two fluids, aqueous and vitreous humors. Aqueous humor fills the anterior chamber of the eye, and vitreous humor fills the posterior chamber of the eye.

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Figure 3–12 Structures of the eye.

The sensory receptors for vision are photoreceptors, which are located on the retina. There are two types of photoreceptors, rods and cones (Table 3-4). Rods have low thresholds, are sensitive to low-intensity light, and function well in darkness. The rods have low acuity and do not participate in color vision. Cones have a higher threshold for light than the rods, operate best in daylight, provide higher visual acuity, and participate in color vision. The cones are not sensitive to low-intensity light.

Table 3–4 Properties of Rods and Cones

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Information is received and transduced by photoreceptors on the retina and then is carried to the CNS via axons of retinal ganglion cells. Some optic nerves cross at the optic chiasm, and others continue ipsilaterally. The main visual pathway is through the dorsal lateral geniculate nucleus of the thalamus, which projects to the visual cortex.

Photoreception

Layers of the Retina

The retina is a specialized sensory epithelium that contains photoreceptors and other cell types arranged in layers. Retinal cells include photoreceptors, interneurons (bipolar cells, horizontal cells, and amacrine cells), and ganglion cells. Synapses are made between cells in two plexiform layers, an outer plexiform layer and an inner plexiform layer. The layers of the retina are described as follows and correspond with the circled numbers in Figure 3-13:

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Figure 3–13 Layers of the retina. The output cells of the retina are the retinal ganglion cells, whose axons form the optic nerves. Circled numbers correspond to layers of the retina described in the text. A, Amacrine cells; B, bipolar cells; G, ganglion cells; H, horizontal cells; R,photoreceptors.

1.     Pigment cell layer. The retina begins just inside the choroid with a layer of pigment epithelium (see Fig. 3-12). The pigment epithelial cells absorb stray light and have tentacle-like processes that extend into the photoreceptor layer to prevent scatter of light between photoreceptors. The pigment cells also convert all-trans-retinal to 11-cis-retinal and deliver the 11-cis form to the photoreceptors (refer to the steps in photoreception).

2.     Photoreceptor layer. The photoreceptors are rods and cones, which consist of a cell body, an outer segment, and an inner segment. Only rods are shown in this figure.

3.     Outer nuclear layer. The nuclei of photoreceptors (R) are contained in the outer nuclear layer.

4.     Outer plexiform layer. The outer plexiform layer is a synaptic layer containing presynaptic and postsynaptic elements of photoreceptors and interneurons of the retina. (The cell bodies of retinal interneurons are contained in the inner nuclear layer.) Synapses are made between photoreceptors and interneurons and also between the interneurons themselves.

5.     Inner nuclear layer. The inner nuclear layer contains cell bodies of retinal interneurons including bipolar cells (B), horizontal cells (H), and amacrine cells (A).

6.     Inner plexiform layer. The inner plexiform layer is the second synaptic layer. It contains presynaptic and postsynaptic elements of retinal interneurons. Synapses are made between retinal interneurons and ganglion cells.

7.     Ganglion cell layer. The ganglion cell layer contains cell bodies of ganglion cells (G), which are the output cells of the retina.

8.     Optic nerve layer. Axons of retinal ganglion cells form the optic nerve layer. These axons pass through the retina (avoiding the macula), enter the optic disc, and leave the eye in the optic nerve.

As mentioned, there are differences in acuity between rods and cones, which can be explained by differences in their retinal circuitry (see Table 3-4). Only a few cones synapse on a single bipolar cell, which synapses on a single ganglion cell. This arrangement accounts for the higher acuity and lower sensitivity of the cones. Acuity is highest in the fovea, where one cone synapses on one bipolar cell, which synapses on one ganglion cell. In contrast, manyrods synapse on a single bipolar cell. This arrangement accounts for the lower acuity but the higher sensitivity of the rods—light striking any one of the rods will activate the bipolar cell.

Structure of the Photoreceptors

Photoreceptors, the rods and cones, span several layers of the retina, as previously described. The outer and inner segments of photoreceptors are located in the photoreceptor layer, the nuclei are located in the outer nuclear layer, and the synaptic terminals (on bipolar and horizontal cells) are located in the outer plexiform layer. The structures of the rods and cones are shown in Figure 3-14.

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Figure 3–14 Structure of photoreceptors. The enlargements show a magnified view of the outer segments.

The outer segments of both rods and cones contain rhodopsin, a light-sensitive pigment (a photopigment). In rods, the outer segments are long and consist of stacks of free-floating double-membrane discs containing large amounts of rhodopsin. The cones have short, cone-shaped outer segments, which consist of infoldings of surface membrane. This infolded membrane also contains rhodopsin, but a smaller amount than is present in the rods. The greater the amount of photopigment, the greater the sensitivity to light, which accounts in part for the greater light sensitivity of the rods. A single photon of light can activate a rod, whereas several hundred photons are required to activate a cone.

The inner segments of the rods and cones are connected to the outer segments by a single cilium. The inner segments contain mitochondria and other organelles. Rhodopsin is synthesized in the inner segments and then incorporated in the membranes of the outer segments as follows: In the rods, rhodopsin is inserted in new membrane discs, which are displaced toward the outer segment; eventually they are shed and phagocytosed by the pigment cell epithelium, giving the outer segments their rodlike shape. In the cones, rhodopsin is incorporated randomly into membrane folds, with no shedding process.

Steps in Photoreception

Photoreception is the transduction process in rods and cones that converts light energy into electrical energy. Rhodopsin, the photosensitive pigment, is composed of opsin (a protein belonging to the superfamily of G protein–coupled receptors) and retinal (an aldehyde of vitamin A). When light strikes the photoreceptors, retinal is chemically transformed in a process called photoisomerization, which begins the transduction process. The steps in photoreception, discussed as follows, correspond to the circled numbers shown in Figure 3-15:

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Figure 3–15 Steps in photoreception. When light impinges on the retina, the photoreceptors are hyperpolarized. In turn, the photoreceptors decrease their release of glutamate, leading to either hyperpolarization or depolarization of bipolar or horizontal cells. Circled numbers correlate with steps described in the text. Cyclic GMP, Cyclic guanosine monophosphate; GMP, guanosine monophosphate.

1.     Light strikes the retina, which initiates photoisomerization of retinal. 11-cis Retinal is converted to all-trans retinal. From there, a series of conformational changes occur in the opsin that culminate in the production of metarhodopsin II. (Regeneration of 11-cis retinal requires vitamin A, and deficiency of vitamin A causes night blindness.)

2.     Metarhodopsin II activates a G protein that is called transducin, or Gt. When activated, transducin stimulates a phosphodiesterase that catalyzes the conversion of cyclic guanosine monophosphate (GMP) to 5′-GMP. Consequently, there is increased breakdown of cyclic GMP, causing cyclic GMP levels to decrease.

3.     and 4. In the photoreceptor membrane, Na+ channels that carry inward current are regulated by cyclic GMP. In the dark, there is an increase in cyclic GMP levels, which produces an Na+ inward current (or “dark current”) and depolarization of the photoreceptor membrane. In the light, there is a decrease in cyclic GMP levels, as already described, which closes Na+ channels in the photoreceptor membrane, reduces inward Na+ current, and produces hyperpolarization.

4.     Hyperpolarization of the photoreceptor membrane decreases the release of glutamate, an excitatory neurotransmitter, from the synaptic terminals of the photoreceptor. (Recall from Figure 3-13 that photoreceptors synapse on bipolar cells and horizontal cells in the outer plexiform layer.)

5.     There are two types of glutamate receptors on bipolar and horizontal cells: ionotropic receptors, which are depolarizing (excitatory), and metabotropic receptors, which are hyperpolarizing (inhibitory). The type of receptor on the bipolar or horizontal cell determines whether the response will be depolarization (excitation) or hyperpolarization (inhibition). Thus, decreased release of glutamate that interacts with ionotropic receptors will result in hyperpolarization and inhibition of the bipolar or horizontal cell (i.e., decreased excitation). And decreased release of glutamate that interacts with metabotropic receptors will result in depolarization and excitation of the bipolar or horizontal cell (i.e., decreased inhibition causes excitation). This process will establish the on-off patterns for visual fields.

Visual Receptive Fields

Each level of the visual pathway can be described by its receptive fields. Thus, there are receptive fields for photoreceptors, bipolar and horizontal cells, ganglion cells, cells of the lateral geniculate body in the thalamus, and cells in the visual cortex. At each higher level, the receptive fields become increasingly complex.

PHOTORECEPTORS, HORIZONTAL CELLS, AND BIPOLAR CELLS

One simple arrangement of visual receptive fields is illustrated in Figure 3-16. The figure shows the receptive fields for three photoreceptors, for two bipolar cells, and for one horizontal cell positioned between the bipolar cells. When light hits the photoreceptors, they are always hyperpolarized and release decreased amounts of glutamate (recall the steps in photoreception), as indicated by the minus signs on the photoreceptors. Photoreceptors synapse directly on bipolar cells in the outer plexiform layer of the retina. The receptive field of the bipolar cell is shown as two concentric circles: The inner circle is called the “center,” and the outer circle is called the “surround.” The center of the bipolar cell’s receptive field represents direct connections from photoreceptors and can be either excited (on) or inhibited (off), depending on the type of glutamate receptor on the bipolar cell, as described earlier. If the center of the receptive field has metabotropic glutamate receptors, then the bipolar cell will be excited (+); if the center of the receptive field has ionotropic glutamate receptors, then the bipolar cell will be inhibited (-). The surround of the bipolar cell’s receptive field receives input from adjacent photoreceptors via horizontal cells. The surround of the receptive field shows the opposite response of the center because the horizontal cells are inhibitory (i.e., they reverse the direct response of the photoreceptor on its bipolar cell). Two patterns for receptive fields of bipolar cells are illustrated in Figure 3-16 and explained as follows:

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Figure 3–16 Visual receptive fields of bipolar cells in the retina. Two patterns are shown: on-center and off-center.

image On-center, off-surround (or “on-center”). This pattern is illustrated in the bipolar cell shown on the left of the figure. The center of its receptive field is excited (on) by light, and the surround of its receptive field is inhibited (off) by light. How is this pattern achieved? As always, light impinging on photoreceptors produces hyperpolarization and decreased release of glutamate. This photoreceptor is connected to the center of the bipolar cell’s receptive field and glutamate binds to a metabotropic receptor. Thus, the center of the receptive field is excited (i.e., decreased inhibition produces excitation). Light also inhibits the adjacent photoreceptor, which binds to an ionotropic receptor in the horizontal cell, thus inhibiting the horizontal cell. The horizontal cell is connected to the surround of the bipolar cell’s receptive field. Because the horizontal cell is inhibited, it reverses the direct action of the photoreceptors on the bipolar cell and produces inhibition in the surround.

image Off-center, on-surround (or “off-center”). This pattern is illustrated in the bipolar cell shown on the right of the figure. The center of its receptive field is inhibited (off) by light, and the surround is excited (on) by light. How is this pattern achieved? Again, light impinging on the photoreceptor produces inhibition. This photoreceptor is connected to the center of the bipolar cell’s receptive field and binds to an ionotropic receptor. Thus, the center of the receptive field is inhibited. Light also inhibits the adjacent photoreceptor, which inhibits the horizontal cell. The horizontal cell is connected to the surround of the bipolar cell’s receptive field. Because the horizontal cell is inhibited, it reverses the direct action of the photoreceptor on the bipolar cell and produces excitation in the surround.

AMACRINE CELLS

The amacrine cells receive input from different combinations of on-center and off-center bipolar cells. Thus, the receptive fields of the amacrine cells are mixtures of on-center and off-center patterns.

GANGLION CELLS

Ganglion cells receive input from both bipolar cells and amacrine cells (see Fig. 3-13). When input to the ganglion cells is primarily from bipolar cells, the ganglion cells retain the on-center and off-center patterns established at the level of the bipolar cells. When the input to a ganglion cell is primarily from amacrine cells, the receptive fields tend to be diffuse because there has been mixing of input at the amacrine cell level.

LATERAL GENICULATE CELLS OF THE THALAMUS

Cells of the lateral geniculate body of the thalamus retain the on-center or off-center patterns transmitted from the ganglion cells.

VISUAL CORTEX

Neurons of the visual cortex detect shape and orientation of figures. Three cell types are involved in this type of visual discrimination: simple cells, complex cells, and hypercomplex cells. Simple cells have receptive fields similar to those of the ganglion cells and lateral geniculate cells (i.e., on-center or off-center), although the patterns are elongated rods rather than concentric circles. Simple cells respond best to bars of light that have the “correct” position and orientation. Complex cells respond best to moving bars of light or edges of light with the correct orientation. Hypercomplex cells respond best to lines of particular length and to curves and angles.

Optic Pathways

The optic pathways from the retina to the CNS are shown in Figure 3-17. Axons from retinal ganglion cells form the optic nerves and optic tracts, synapse in the lateral geniculate body of the thalamus, and ascend to the visual cortex in the geniculocalcarine tract.

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Figure 3–17 Optic pathways. Fibers from the temporal visual fields cross at the optic chiasm, but fibers from the nasal visual fields remain uncrossed. (Modified from Ganong WF: Review of Medical Physiology, 20th ed. Norwalk, Conn, Appleton & Lange, 2001.)

Notice that the temporal visual fields project onto the nasal retina, and the nasal fields project onto the temporal retina. Nerve fibers from each nasal hemiretina cross at the optic chiasm and ascend contralaterally. Nerve fibers from each temporal hemiretina remain uncrossed and ascend ipsilaterally. Thus, fibers from the left nasal hemiretina and fibers from the right temporal hemiretina form the rightoptic tract and synapse on the right lateral geniculate body. Conversely, fibers from the right nasal hemiretina and fibers from the left temporal hemiretina form the left optic tract and synapse on the left lateral geniculate body. Fibers from the lateral geniculate body form the geniculocalcarine tract, which ascends to the visual cortex (area 17 of the occipital lobe). Fibers from the right lateral geniculate body form the right geniculocalcarine tract; fibers from the left lateral geniculate body form the left geniculocalcarine tract.

Lesions at various points in the optic pathway cause deficits in vision, which can be predicted by tracing the pathway, as shown in Figure 3-18Hemianopia is the loss of vision in half the visual field of one or both eyes. If the loss occurs on the same side of the body as the lesion, it is called ipsilateral; if the loss occurs on the opposite side of the body as the lesion, it is called contralateral. The following lesionscorrespond to the shaded bars and circled numbers on the figure:

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Figure 3–18 Visual field defects produced by lesions at various levels of the visual pathway. Circled numbers refer to deficits and are explained in the text. (Modified from Ganong WF: Review of Medical Physiology, 20th ed. Norwalk, Conn, Appleton & Lange, 2001.)

1.     Optic nerve. Cutting the optic nerve causes blindness in the ipsilateral (same side) eye. Thus, cutting the left optic nerve causes blindness in the left eye. All sensory information coming from that eye is lost because the cut occurs before any fibers cross at the optic chiasm.

2.     Optic chiasm. Cutting the optic chiasm causes heteronymous (both eyes) bitemporal (both temporal visual fields) hemianopia. In other words, all information is lost from fibers that cross. Thus, information from the temporal visual fields from both eyes is lost because these fibers cross at the optic chiasm.

3.     Optic tract. Cutting the optic tract causes homonymous contralateral hemianopia. As shown in the figure, cutting the left optic tract results in loss of the temporal visual field from the right eye (crossed) and loss of the nasal visual field from the left eye (uncrossed).

4.     Geniculocalcarine tract. Cutting the geniculocalcarine tract causes homonymous contralateral hemianopia with macular sparing (the visual field from the macula is intact). Macular sparing occurs because lesions of the visual cortex do not destroy all neurons that represent the macula.