Transient Receptor Expression in Visual Cortex Development and the Mechanisms of Cortical Plasticity

Abstract

During the first few months of postnatal life, the kitten visual cortex exhibits a remarkable plasticity, enabling it to match its organization to the visual environment with which it is confronted. If the visual environment is abnormal, as occurs with early monocular cataract or refractive error, then binocular competition results, with the eye that sees less well permanently losing cortical territory to the non-deprived eye (Cynader and Chernenko, 1976; Wiesel and Hubel, 1963a; Wiesel and Hubel, 1965). This binocular competition occurs only during a well-defined critical period which begins about three weeks after birth, peaks sharply between four and six weeks of age, and then declines slowly until the animal is about six months of age (Cynader et al., 1980; Hubel and Wiesel, 1970). We have investigated the mechanisms underlying binocular competition and the critical period that underlies it. In a series of electrophysiol-ogical experiments that have been described in detail elsewhere, the following features of binocular competition are now well established: (a) Binocular competition involves changes at the level of the lateral geniculate nucleus (LGN) (Wiesel and Hubel, 1963b), the terminals of LGN afferents in the cortex (Hubel et al., 1977) and in the responses of cortical cells (Wiesel and Hubel, 1963a), but the primary event in binocular competition appears to involve the responses of the postsynaptic cells in Layer IV. This has been established by investigations showing that binocular competition can be made to be completely orientation dependent (Cynader and Mitchell, 1977), a property of cortical cells and not their afferents (Hubel and Wiesel, 1962), and by experiments which involve selective excitation (Shaw and Cynader, 1984) or inhibition (Reiter and Stryker, 1988) of cortical cells. In these latter experiments it has been shown that disturbing the responsivity of cortical cells without affecting the asymmetric input from the LGN that occurs with monocular suture is sufficient to prevent the effects of monocular deprivation.