Abstract

The effects of prolonged monocular deprivation (MD) on horizontal optokinetic nystagmus (OKN) have been examined in cats subjected to unilateral or bilateral visual cortex lesions. Presurgically, OKN elicited through the deprived eye was substantially weaker than that through the non-deprived eye. This effect was most prominent for OKN in response to temporalward stimulation, which essentially was abolished in the deprived eye. In addition, OKN elicited by temporalward stimulation of the non-deprived eye tended to be weaker in comparison to nasalward stimulation of that eye. A bilateral cortical lesion severely disrupted OKN behavior through the non-deprived eye but left OKN through the deprived eye relatively unaffected, with the result that the marked interocular differences in OKN that were present presurgically disappeared. During the recovery period following this lesion, there was a small gradual improvement in OKN through both eyes, so that OKN performance through the deprived eye ultimately exceeded that observed presurgically. Unilateral cortical lesions had little effect on OKN through the deprived eye, but they produced substantial changes in OKN through the non-deprived eye. Both the immediate effects of cortical lesions, and the patterns of recovery observed following these lesions, in many ways resemble those observed when normally reared cats are subjected to similar lesions. These behavioral experiments indicate that while subcortical OKN pathways are spared from the effects of long-term monocular deprivation, cortical pathways mediating OKN through the deprived eye are severely disrupted.

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