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Abstract
Mild hypoxia elevates the standing potential and alters three slow components of the DC electroretinogram in the cat: the c-wave, the fast-oscillation trough, and the light peak. This paper considers the cellular mechanisms of these effects. Elevation of the standing potential results from a depolarization of the basal membrane of retinal pigment epithelial (RPE) cells. The depolarization is indirectly initiated by an elevation of [K+]0 in the subretinal space during hypoxia, and is accompanied by a decrease in basal membrane resistance that leads to an increase in the c-wave. There is also some evidence that hypoxia may alter the standing potential by directly affecting the basal membrane of the RPE. The fast-oscillation trough, which follows the c-wave when illumination is maintained, deepens during hypoxia. This is caused primarily by an increase in the amplitude of the delayed hyperpolarization of the RPE basal membrane that results from a slowing of the rate of recovery of light-evoked [K+]0 during hypoxia. The changes in [K+]0 probably result, in turn, from a decrease in the rate of the photoreceptors' Na+/K+ pump. The light peak's amplitude is reduced during hypoxia and its time-to-peak is lengthened, and this may be related to a change in photoreceptor metabolism that is distinct from the effect on the Na+/K+ pump. Knowledge of these mechanisms may eventually enhance the clinical usefulness of the standing potential and the c-wave, fast-oscillation, and light peak.