Abstract
In a series of landmark experiments, Hubel and Wiesel (1963) demonstrated that the development of primary visual cortex could be disrupted by a variety of sensory perturbation. If a mammal is monocularly deprived (MD) of vision for several days during the early period of postnatal development, the animal permanently becomes ambliopic in that eye (Baker et al., 1974; Boothe et al., 1985; Domenici et al., 1991). The visual acuity of the deprivated eye is decreased and its contrast sensitivity depressed. Most visual cortical neurones become unresponsive to visual stimulation of the deprived eye and the ocular dominance distribution of cells shifts in favour of the eye receiving normal visual input (Giffin and Mitchell, 1978; Harwerth et al., 1989; Domenici et al., 1991a, c). Anatomically, MD performed during the critical period determined the reduction of the territories occupied in the primary visual cortex by the afferents from the deprived laminae of the LGN and the expansion of the territories occupied by the terminals from the non deprived laminae. There is also a shrinkage of the soma size of LGN projection cells in the binocular portion of the deprived laminae (Shatz and Stryker, 1978; LeVay et al., 1980; Guillery and Stelzner, 1970; Sherman et al., 1974).
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Fagiolini, M., Pizzorusso, T., Maffei, L. (1995). Visual Cortical Plasticity and Neurotrophic Factors. In: Robbins, J.G., Djamgoz, M.B.A., Taylor, A. (eds) Basic and Clinical Perspectives in Vision Research. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9362-8_15
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