Abstract

The late RP (receptor potential) was isolated in macaque monkeys by clamping the retinal circulation at the optic disc, while maintaining the animal on light halothane anesthesia with well controlled arterial oxygenation. Just after its isolation the late RP from all retinal areas was pure cone in origin, when elicited by stimulus intensities well above cone threshold. This was shown by criteria of response form, and by spectral response curves. In the central fovea and parafovea these pure cone responses were well maintained. At constant photopic intensity, however, a slowly decaying rod contribution appeared in the late RP of the peripheral retina soon after clamping the retinal circulation. This was shown to result from hypoxia of the peripheral retina, and the response that appeared was shown of rod origin by criteria of response form, spectral response curves, its selective abolition by adaptation with white light, and its recovery rate after light adaptation. After its appearance by hypoxia, the rod late RP was present throughout the photopic intensity range. In another series of experiments the late RP was isolated by infusing pentobarbital into the vitreous humor. At concentrations just sufficient to isolate the late RP, responses to photopic intensities were pure cone. At higher concentrations a rod contribution appeared in both the response form and the spectral response curve, and this effect was reversible. With either method of isolating the late RP, a pure rod late RP could always be seen by lowering stimulus intensity into the scotopic range. Our results indicate that under normal physiological conditions, stimuli well above cone threshold do not elicit a rod response of saturated amplitude; instead, the rod late RP is completely suppressed. At photopic intensities where visual functions are mediated only by cones, the entire post-receptor pathway is thus cleared for carrying pure cone signals. This mechanism has advantages or implications for many aspects of photopic visual functions. It appears to result from a lateral inhibitory pathway initiated by cones and involving the horizontal cell as inhibitory interneuron, with this pathway being functionally interrupted by either hypoxia or pentobarbital.

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