It seems paradoxical that V1 receptive field development passively follows peripheral organization, which is not influenced by visual experience in primates (Blakemore and Vital-Durand, 1986b; Hendrickson et al., 1987; Levitt et al., 2001; Movshon et al., 1987), whereas decades of evidence has accumulated for experience-dependent plasticity in V1. Most studies of the effect of visual experience on development in primates have used monocular or binocular deprivation to manipulate visual experience (Baker et al., 1974; Blakemore, 1990; Blakemore and Vital-Durand, 1986b; Horton, 1984; LeVay et al., 1980; von Noorden and Crawford, 1978; Wiesel, 1982; Wiesel and Hubel, 1974). This kind of deprivation typically devastates spatial vision, reducing contrast sensitivity and resolution so severely that in some cases blindness results (Harwerth et al., 1983; von Noorden, 1973; von Noorden et al., 1970). The most obvious consequence of monocular deprivation is a dramatic loss of influence of the deprived eye over cells in the visual cortex, evident physiologically and anatomically, even when the deprivation lasts for as short a period as 1 week. Physiologically, cortical binocularity is lost, and most neurons can be influenced only through the nondeprived eye. Anatomically, there is a nearly complete takeover of deprived eye territory by the nondeprived eye.
The obvious correlation between the loss of cortical influence by the deprived eye and the loss of vision has been interpreted to mean that visual function is determined by the number of cortical neurons influenced by a given eye; changes in this balance during development lead to changes in vision. None of these studies has quantified the spatial, temporal, or contrast response properties of deprived cortex, as there are few responsive cells to study. It may be that experience-dependent plasticity in primate V1 is restricted to the balance of inputs from the two eyes, and does not affect the spatial properties of individual neurons. But data on the effects of binocular deprivation suggest that cortical receptive field properties can be altered by experience (Blakemore, 1990). We wanted to establish whether cortical receptive field properties could be influenced by abnormal visual experience that was less radical than complete form deprivation, and we have therefore studied visual behavior and cortical organization in animals raised in a way that creates more modest and experimentally tractable visual deficits.
Visual disorders that occur in early childhood, such as strabismus (crossed eyes) and anisometropia (monocular defocus), are associated with amblyopia, literally meaning "blunted" vision. Visual acuity and contrast sensitivity in the amblyopic eyes of monkeys and humans are reduced, but not nearly so severely as they are following visual deprivation (Blakemore and Vital-Durand, 1981; Harwerth et al., 1983; Kiorpes, 1992b, 1996, 2001; Kiorpes et al., 1987; Kiorpes et al., 1993; Kiorpes and Movshon, 1996; Levi and Carkeet, 1993; Smith et al., 1985). Figure 12.7A shows the development of spatial resolution in each eye of a population of strabismic monkeys (Kiorpes, 1992b) and compares it to the development of resolution in normal monkeys tested monocularly. Resolution in the fellow (nondeviating) eyes develops normally, but resolution development in the strabismic eyes lags. Figure 12.7B illustrates losses in contrast sensitivity for three monkeys, each made experimentally amblyopic by a different technique. Normally, contrast sensitivity is similar for both eyes of an individual (upper left panel, TJ). The other three panels show contrast sensitivity for each eye in monkeys in which the development of amblyopia followed experimentally produced strabismus, blur created by extended wear of a defocusing contact lens (ani-sometropia), or blur created by chronic instillation of atropine. Contrast sensitivity functions for the amblyopic eyes, regardless of the origin of amblyopia, are shifted to lower sensitivity and lower spatial frequencies. If we compare the functions obtained from amblyopic eyes with functions from young normal animals (Fig. 12.2B). There is sa
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