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Vito Scavetta, David G. Jones, Donald E. Mitchell, Kathryn M. Murphy; NMDA-dependent recovery of visual acuity following monocular deprivation. Journal of Vision 2002;2(7):24. doi: 10.1167/2.7.24.
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Monocular deprivation leads to anatomical and physiological changes in the visual cortex, as well as reduced visual acuities. These changes can be ameliorated by reverse occlusion. The visual and physiological recovery, however, is labile and results in poor vision in both eyes — bilateral amblyopia (Murphy & Mitchell, 1986). The underlying causes of these behavioral and physiological results have been a puzzle, however, the visuotopic loss of NMDA expression in the visual cortex promoted by monocular deprivation provides some clues. We initiated a series of studies to determine the rearing conditions that promote recovery of NMDA expression and whether those conditions would lead to permanent recovery of visual acuity. Kittens were reared with various regimens of monocular deprivation and reverse occlusion by eyelid suture. The tangential pattern of NMDAR1 immunostaining was analyzed in supragranular sections from unfolded and flattened visual cortex. Visual acuity was measured using the jumping stand. We found that reverse occlusion alone did not promote recovery of NMDAR1 expression, however, just 4 days of binocular vision after monocular deprivation did promote recovery of NMDAR1. We designed a new rearing regimen, based on the role of NMDA in long-term plasticity in the visual cortex, that promoted both recovery of NMDAR1 expression and permanent recovery of visual acuity after reverse occlusion. These results suggest that NMDA expression is required for permanent recovery of visual acuity and provide a key piece to solving the puzzle of bilateral amblyopia.
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