Cellular activities of the retina are discussed in relation to the maintenance of the internal environment of the organ and the preservation of cell life, including the most important manifestation of disturbed retinal cell life, the degeneration of the visual cells on a hereditary basis. In regard to the former activities, the role of the “nonneuronal” cells is stressed, especially that of the pigment epithelium which seems to be the site of generation of a major fraction of the steady (dc) potential across the mammalian retina, and also of the “slow” potentials resulting from changes in retinal illumination. A new technique permitting the measurement of transretinal currents at constant (“clamped”) voltages and of transretinal ion fluxes is described. Preliminary experiments indicate that the dc potential originates from differences in active and passive potassium ion movements through the two planar surfaces of the pigment epithelium. Structural differences of these surface regions are related to the experimental findings, and the pigment epithelium is viewed as a “living barrier” between body and visual cell layers. Bruch’s membrane, to which much importance has been attached by others in relation to electrical phenomena, is considered to provide “mechanical” support for the retina, its electrophysiological properties to be negligible in first approximation relative to those of the plasma membrane of the pigment epithelial cell. The main energetic support of the retinal cells derives from the catabolism of glucose, its degradation to lactic acid and oxidation mainly by the citric acid cycle. A deficiency in energy-yielding processes of glucose metabolism is not the basic abnormality which leads, on a hereditary basis, to visual cell death during the first weeks (or months) of the postnatal life in certain mouse and rat strains. Phenomena of this disease are described from various points of view, and it is emphasized that a deficiency in rhodopsin synthesis does not exist; on the contrary, retinal rhodopsin concentration increases while the visual cells deteriorate functionally. The genetic abnormality seems to involve primarily a control factor that directs by unknown mechanisms visual cell development and differentiation to the functional state.
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