Observations on monocular deprivation in mice

Publisher Website
Google Scholar
Abstract
In normal mouse striate cortex the geniculocortical projections subserving input from the 2 eyes appeared to be evenly mixed in layer IV: there was no indication of tangential or radial segregation of ocular inputs either from physiological recordings or morphologically with transneuronal autoradiography after injecting an eye with tritiated proline. In normal mice both anatomical and physiological evidence indicated that the input from the contralateral eye was dominant in the binocular region. Physiologically the contralateral-to-ipsilateral ratio was about 2-1. In mice raised with 1 eyelid closed the physiologically recorded ocular-dominance distributions of cells in area 17 showed drastic changes. In the hemisphere contralateral to the deprived eye the majority of cells could still be driven through either eye; the ipsilateral experienced eye was on the whole dominant. In the cortex ipsilateral to the deprived eye this eye had lost almost all of its influence on cortical cells in favor of the contralateral experienced eye. With transneuronal autoradiography no obvious anatomical changes were observed in the monocularly deprived cortex. The geniculocortical projections appeared roughly normal after injection of either the deprived eye or the eye that was open. As an explanation for the seeming contradiction between physiological and morphological results, it was assumed that through monocular deprivation the projection from the deprived eye to the cortex ipsilateral to that eye had become nonfunctional but was morphologically still present. To test this assumption of a nonfunctional projection the experiment of Kratz, Spear and Smith was repeated in mice in an effort to restore activity in the deprived eye. In adult monocularly deprived mice the experienced eye was enucleated and cells in the binocular area ipsilateral to the remaining eye were studied for visual input. No unequivocal changes were seen either immediately or within a few hours of eye enucleation. In the following days and weeks visual responses appeared and increased until practically all cells in the upper cortical layers reacted to visual stimulation. Cells in and deep to the lower part of layer V remained unresponsive. While showing recovery, the cortex on the whole seemed abnormal; the more elaborate receptive-field types seen in normal mouse cortex were missing.