Figure 2313

Electron micrograph of the retinal pigment epithelium in association with the outer segments of rods and cones. Retinal pigment epithelial cells (RPE) contain numerous elongated melanin granules that are aggregated in the apical portion of the cell, where the microvilli extend from the surface toward the outer segments of the rod and cone cells. The retinal pigment epithelial cells contain numerous mitochondria and phagosomes. The arrow indicates the location of the junctional complex between two adjacent cells, x20,000. (Courtesy of Dr. Toichiro Kuwabara.)

The outer nuclear layer (4) contains the nuclei of the retinal rods and cones

The region of the rod cytoplasm that contains the nucleus is separated from the inner segment by a tapering process of the cytoplasm. In cones, the nuclei are located close to the outer segments, and no tapering is seen. The cone nuclei stain lightly and are larger and more oval than rod nuclei. Rod nuclei are surrounded by only a thin rim of cytoplasm. In contrast, a relatively thick investment of cytoplasm surrounds the cone nuclei (see Fig. 23.11).

The outer plexiform layer (5) is formed by the processes of the photoreceptor cells and neurons

The outer plexiform layer is formed by the processes of retinal rods and cones and the processes of horizontal, amacrine, and bipolar cells. The processes allow the electrical coupling of photoreceptor cells to these specialized interneurons via synapses. A thin process extends from the region of the nucleus of each rod or cone to an inner expanded portion with several lateral processes. The expanded portion is called a spherule in a rod and a pedicle in a cone. Normally, many photoreceptors converge onto one bipolar cell and form interconnecting neural networks. Cones located in the fovea, however, synapse with a single bipolar cell. The fovea is also unique in that the compactness of the inner neural layers of the retina causes the photoreceptors to be oriented obliquely. Horizontal cell dendritic processes synapse with photoreceptors throughout the retina and further contribute to the elaborate neuronal connections in this layer.

The inner nuclear layer (6) consists of the nuclei of horizontal, amacrine, bipolar, and Müller s cells

Müller's cells form the scaffolding for the entire retina. Their processes invest the other cells of the retina so completely that they fill most of the extracellular space. The basal and apical ends of Müller's cells form the inner and outer limiting membranes, respectively. Microvilli extending from their apical border lie between the photoreceptors of the rods and cones. Capillaries from the retinal vessels extend only to this layer. The rods and cones carry out their metabolic exchanges with extracellular fluids transported across the blood-retina barrier of the RPE.

The three types of conducting cells—bipolar, horizontal, and amacrine—found in this layer have distinct orientations (see Fig. 23.9). The processes of bipolar cells extend to both the inner and outer plexiform layer. Through these connections, the bipolar cells establish synaptic connections with multiple cells in each layer except in the fovea, where the number of interconnected cells is reduced to provide greater visual acuity. The processes of horizontal cells extend to the outer plexiform layer where they intermingle with processes of bipolar cells. The cells have synaptic connections with rod spherules, cone pedicles, and bipolar cells. This electrical coupling of cells is thought to affect the functional threshold between rods and cones and bipolar cells. The processes of amacrine cells branch extensively to provide sites of synaptic connections with axonal endings of bipolar cells and dendrites of ganglion cells.

In the peripheral regions of the retina, the axons of bipolar cells pass to the inner plexiform layer where they synapse with several ganglion cells. In the fovea, they may synapse with a single ganglion cell, again reflecting the greater visual acuity in this region. Amacrine cell processes pass inward, contributing to a complex interconnection of cells. They synapse in the inner plexiform layer with bipolar, ganglion, and other amacrine cells (see Fig. 23.9).

The inner plexiform layer (7) consists of a complex array of intermingled neuronal cell processes

The inner plexiform layer consists of a complex intermingling of the processes of the amacrine, bipolar, and ganglion cells. The course of these processes is parallel to the inner limiting membrane, thus giving the appearance of horizontal striations to this layer (see Fig. 23.10).

The ganglion cell layer (8) consists of the cell bodies of large multipolar neurons

The cell bodies of large multipolar nerve cells, measuring up to 30 fxm in diameter, constitute the ganglion cell layer. These nerve cells have lightly staining round nuclei with prominent nucleoli and have Nissl bodies in their cytoplasm. An axonal process emerges from the rounded cell body, passes into the nerve fiber layer, and then goes into the optic nerve. The dendrites extend from the opposite end of the cell to ramify in the inner plexiform layer. In the peripheral regions of the retina, a single ganglion cell may synapse with a hundred bipolar cells. In marked contrast, in the macular region surrounding the fovea, the bipolar cells are smaller (some authors refer to them as "midget" bipolar cells), and they tend to make one-to-one connections with ganglion cells. Over most of the retina, the ganglion cells are only a single layer of cells. At the macula, however, they are piled up to eight deep, although they are absent over the fovea itself. Scattered among the ganglion cells are small neuroglial cells with densely staining nuclei (see Fig. 23.10).

The layer of optic nerve fibers (9) contains axons of the ganglion cells

The axonal processes of the ganglion cells form a flattened layer running parallel to the retinal surface. This layer increases in depth as the axons converge at the optic disc. The axons are thin, nonmyelinated processes measuring up to 5 /xm in diameter (see Fig. 23.10).

Age-related macular degeneration (ARMD) is the most common cause of blindness in older individuals. Although the etiology of this disease is still unknown, evidence suggests both genetic and environmental (UV irradiation, drugs) components. The disease causes loss of central vision, while peripheral vision remains unaffected. Two forms of ARMD are recognized: a dry (atrophic, nonexudative) form and a wet (exudative, neovascular) form. The latter is considered a complication of the first. Dry ARMD is the most common form (90% of all cases) and involves degenerative lesions localized in the area of the macula lutea. The degenerative lesions include a focal thickening of Bruch's membrane called "drusen," atrophy and depigmentation of RPE, and obliteration of capillaries in the underlying chorioid layer. These changes lead to deterioration of the overlying photosensitive retina, resulting in the formation of "blind spots" in the visual field (Fig. 23.14). Wet ARMD is a complication of dry ARMD caused by neovascularization of "blind spots" of the retina in the large drusen. These newly formed, thin, fragile vessels frequently leak and produce exudates and hemorrhages in the space just beneath the retina, resulting in fibrosis and scarring. These changes are responsible for the progressive loss of central vision over a short time. The treatment of wet ARMD includes conventional laser treatment therapy; however, new surgical methods such as macular translocation have been recently introduced. In this procedure, the retina is detached, translocated, and reattached in a new location, away from the chorioid neovascular tissue. Conventional laser treatment is then applied to destroy pathologic vessels without destroying central vision.

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