Abstract
Vision is immature in newborns of virtually every species studied. Vision develops over some protracted period of time, the duration of which depends on the species. During this developmental period, the visual system is vulnerable to abnormal visual experience. Many studies over the past 25 years have sought to define the nature of this “critical period”. However, the critical period is in fact a concept that subsumes many types of vulnerability, for example, susceptibility to insult as well as responsiveness to treatment (Daw, 1998). Different aspects of visual function have different critical periods. For example, spectral sensitivity has a very early, relatively short sensitive period whereas binocular vision has a very long one (Harwerth et al., 1986). Different structures in the visual pathways also have different critical periods. This is evident, for example, from studies showing that many years of monocular deprivation has little functional consequence for neurons in the lateral geniculate nucleus of monkeys (Levitt et al., 2001), yet has devastating consequences for neurons in primary visual cortex.
This talk will review some of what we know about critical periods and the development of amblyopia (reduced acuity resulting from early strabismus, blur, or deprivation) from work with animal models. In particular, I will discuss the evidence that differential vulnerability of visual function arises from the nature of the neural mechanisms underlying those visual functions. The implications for the treatment of amblyopia will be addressed.