Binocular signal interactions in the primary visual cortex of macaque monkeys reared with early abnormal visual experience

Chronically uncorrelated signals from the two eyes early in life have devastating effects on binocular visual development. In humans, congenital cataract, early strabismus, or early anisometropia are known to lead to permanent binocular vision deficits and often amblyopia. Animal models of binocular vision disorders have been employed to investigate how sensory deficits emerge in human infants and to facilitate the development of effective treatment strategies.; In the first project, I investigated the effects of early strabismus by focusing on how the onset age and the duration of optically induced strabismus affect the severity of binocular response deficits in monkey V1. I found that (1) two weeks of optical strabismus after 4 weeks of age resulted in a higher prevalence of binocular suppression and clear reductions in the neuronal sensitivity to interocular spatial phase disparity than did strabismus before 4 weeks of age, (2) only 3 days of optical strabismus was sufficient to cause a large scale interocular suppression without affecting disparity sensitivity, (3) 7 days of misalignment caused both disparity sensitivity loss and increased suppression while the severity of these deficits was less than that after 14 days of optical strabismus, and (4) the durations longer than 2 weeks had no additional impact.; In the second project, I investigated the effects of alternating defocus on the development of binocular connections in the visual cortex. It was found that neuronal sensitivity to interocular spatial phase disparity was reduced in lens-reared monkeys, and that this reduction was generally more severe for units tuned to higher spatial frequencies. These results support the hypothesis that the local disparity processing mechanisms in primates are spatially tuned and can be independently compromised by early abnormal visual experience.; In the third project, I compared the binocular response deficits in monkey visual cortex (V1) resulting from daily alternating monocular form deprivation (alternating occlusion). Both early alternating occlusion and strabismus severely disrupted the binocular connections in the primary visual cortex of monkeys. Consequently, the proportion of binocularly balanced cells and the disparity sensitivity of V1 units were severely reduced, and neurons exhibiting large binocular facilitatory interactions were rarely encountered. However, while the residual binocular interactions in V1 of strabismic monkeys were dominated by interocular suppression under dichoptic conditions, the proportion of units with large binocular suppression was very small in occluder-reared monkeys. (Abstract shortened by UMI.)...