What's critical for the critical period in visual cortex?

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Abstract

regions representing the closed eye, and expansion of Durham, North Carolina 27710 those representing the open eye (Figure 1B). While in normal primates and cats, the thalamic inputs represent-ing the two eyes parse cortical layer 4 into alternating, equal-sized stripes, eye closure during the critical period During a brief period in postnatal life, sensory experi-ences indelibly shape the behavior of many vertebrate reduced the cortical territory of the closed eye to species. Salmon learn their natal rivers, birds learn their shrunken broken stripes, with its former territory now father's songs, and humans acquire language based invaded by inputs representing the other eye (Hubel et on particular sensory experiences during such " critical al., 1977). Behaviorally, animals monocularly deprived periods. " Early ethological investigations of critical peri-ods focused on the behavioral consequences of early sensory experiences, but how and where such experi-ences were permanently etched into brain circuits was unknown. The notion that critical periods actually repre-sented heightened epochs of brain plasticity, and that ex-perience could produce permanent, large-scale changes in neuronal circuits emerged from Hubel and Wiesel's investigations in the cat and monkey visual cortex begin-ning in the mid-1960s (Hubel and Wiesel, 1970). Despite over three decades of subsequent experimentation, passionate disagreement remains over the cellular and molecular mechanisms initiating and eventually termi-nating this brief period of remarkable plasticity. For years, the battle was waged using pharmacologi-cal manipulations in the visual system of cats and pri-mates. Recently, however, genetic manipulations in the mouse have emerged as a powerful new tool for dis-secting the molecular underpinnings of critical periods. Two recent reports, using very different genetic manipu-lations, highlight the development of inhibitory circuitry as a potent modulator of the critical period, although in the best tradition of this contentious area, they reach rather different conclusions. In one case transgenic over-expression of a neurotrophin has made it possible, for the first time, to prematurely close the critical period (Huang et al., 1999); in another other case, critical period plasticity was disrupted in a knockout mouse and subse-quently restored with a specific pharmacological agent Figure 1. The Visual Systems of Cat and Mouse and Their Re-(Hensch et al., 1998a). Both the findings themselves sponses to Monocular Deprivation during the Critical Period and the mice engineered to obtain them offer a wealth In cats (and primates) the projections from the ipsilateral (red) and of new opportunities to delve more precisely into the contralateral (green) portions of the two retinas segregate into ana-molecular mechanisms regulating this unique time in tomically discrete layers in the visual thalamus (LGN). LGN neurons vertebrate brain development. from each layer project in turn to segregated zones in layer 4 of primary visual cortex, forming alternating bands that comprise the In their classic work, Hubel and Wiesel discovered anatomical basis of ocular dominance columns. In contrast, mice that neurons in cat primary visual cortex were activated have a much smaller projection from the ipsilateral retina, and to different degrees by visual stimuli presented to one the projections from the two eyes do not form distinct layers in the eye or the other, a property they termed ocular domi-LGN or segregated bands in cortex. In cats, eye closure of the nance. They then made the striking discovery that clos-contralateral eye (indicated the shading in [B]) causes the thalamic ing one eye during the first few months of life led to the afferents to the cortex representing that eye to shrink, while the lifelong, irreversible loss of visually driven activity in the afferents representing the open eye expand. In mice, more subtle changes in individual axon arbors have been observed. Physiologi-cortex through the closed eye, and a dramatic increase cally (C) most cells are activated to some extent by both eyes in in the number of neurons responding best to stimuli normal animals (left histograms); eye closure at the height of the presented to the open eye (Figure 1C) (Hubel and Wiesel, critical period results in a dramatic loss of neurons reponsive to 1970). This was all the more remarkable because re-the closed eye. This shift is somewhat more dramatic in cats and sponses in the deprived retina and thalamus remained monkeys than in mice, but qualitatively similar. (Figure is modified completely unaffected. In contrast to the profound ef-from Wiesel and Hubel, 1970 and earlier references therein, and Gordon and Stryker, 1996.) fects in young animals, even prolonged eye closure in

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Katz, L. C. (1999, December 23). What’s critical for the critical period in visual cortex? Cell. Cell Press. https://doi.org/10.1016/S0092-8674(00)81665-7

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