Visual Deprivation in Monkeys: its Effects and its Reversal

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The well-established anatomical and physiological sequelae of monocular visual deprivation in the primate brain can be reversed by forced usage of the deprived eye, although it seems that the good eye must be occluded for this to be effective in the relatively simple paradigm used here. The possible reversal of an experimental deprivation condition is obviously of considerable importance in the clinical treatment of childhood amblyopia. Unilateral eyelid closure in kittens or baby monkeys causes most visual cortical neurons to become unresponsive to the deprived eye. In kittens, “reverse suture” leads to “recapture” of cortical cells by the initially deprived eye, if done sufficiently early. In the monkey also, reverse suture causes total recapture if done early with expansion of the ocular dominance “columns” in layer IVc of area 17 related to the newly opened eye. Late reversal is ineffective and intermediate reversal causes partial recapture.Monocular deprivation also affects normal cell growth in the lateral geniculate nucleus (LGN) of monkeys, such that the neurons innervated by the deprived retina are smaller than normal. Reverse suture in kittens leads to a recovery of cell size in the initially deprived LGN laminae and to a shrinkage in the others. In the monkey, monocular deprivation leads to less effect on LGN cells than in the cat; reverse suture results in recovery of LGN cell size.

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