Studies of experimental amblyopia have revealed two major physiological changes which correlate with the monocular acuity loss: suppression of input from one eye in the visual cortex and decreased spatial resolving power in cells of the lateral geniculate nucleus which are driven by the amblyopic eye. Unravelling the relative importance of these changes in non-deprivation forms of amblyopia (strabismic, anisometropic) has been hampered by the lack of appropriate animal models. Recently, we have developed a non-deprivation animal model of amblyopia which reliably produces both physiological effects without monocular forms or light deprivation. This model puts us uniquely in a position to systematically analyze non-deprivation amblyopia. We propose a series of comparative studies using this model as well as more traditional ones (monocular deprivation, surgical strabismus). Specific goals include: 1) to clarify the etiology of amblyopia by creating environments in which different visual factors (defocused images, conflicting visual input) can be studied in isolation; 2) to assess whether cortical or geniculate physiological changes correlate better with the acuity loss by a combination of behavioral and physiological techniques; 3) to assess the role of binocular competition in non-deprivation amblyopia by evaluating whether the amblyopic deficit depends upon the visual experience of the other eye. 4) to better define the primary locu of the neural changes in amblyopia by a combination of anatomical and physiological techniques; 5) to assess the role of inhibition in the physiological changes of non-deprivation amblyopia by iontophoretic application of disinhibiting agents (bicuculline, naloxone) 6) to determine if disinhibition can restore useful vision to an amblyopic eye by a combination of behavioral and evoked cortical potential techniques.