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I. Maruko, I. Watanabe, B. Zhang, J. Zheng, H. Bi, J. Wensveen, E.L. Smith, Y.M. Chino; Binocular response properties of V1 and V2 neurons in monkeys reared with early monocular form deprivation and brief unrestricted vision. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):5494.
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Purpose: Monocular form deprivation early in life leads to a dramatic loss of binocularly driven cortical neurons and behaviorally demonstrated form–deprivation amblyopia. However, we previously reported that brief daily periods of unrestricted vision during monocular form deprivation can prevent or reduce the impact of amblyopia. In this study we determined whether or not the binocular response properties of V1 and V2 neurons of these monkeys were altered. Methods: Six infant macaque monkeys were reared with monocular diffuser between 3 weeks and 4 months of age. The rearing regimen included daily unrestricted vision for one, two or four hours. Upon completion of the behavioral testing to determine if the monkeys exhibited amblyopia, we conducted the microelectrode recording experiments to measure the disparity sensitivity of individual units and the prevalence of binocular suppression in V1 and V2. Results: There was a clear loss of binocularly balanced cells in both V1 and V2 of monkeys reared with one hour of normal vision. Ocular dominance distribution of V2, but not V1units, was shifted in favor of the non–deprived eye. Monkeys reared with 4 hours of normal vision did not have any loss of binocular cells in either V1 or V2. Monkeys reared with 2 hours of unrestricted vision showed a slight reduction in units dominated by the deprived eye. However, in all treated groups, there were significant reductions in the disparity sensitivity and anomalous increases in binocular suppression. The duration of unrestricted vision did not affect the severity of these binocular response deficits in either V1 or V2. Conclusions: These results suggest that the developing binocular connections in V1 and V2 are exceedingly sensitive to binocularly uncorrelated signals and thus, earlier or more complete intervention is necessary to prevent binocular response deficits from emerging.
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