Amblyopia is a major concern in pediatric ophthalmology. Roughly 3% of children develop amblyopia, a developmental disorder of vision. Amblyopia is a deficit in vision that is not due to any obvious pathology but is not correctable by spectacle lenses. It is known to be associated with cataracts, strabismus, and blur, when they occur during childhood. If amblyopia is not detected and corrected during childhood, the deficits become permanent. We study animal models to carefully control the visual histories of the subjects, to be confident of the causality of the amblyopia, and to study the neurobiological correlates of visual behavior directly in the same species. We study the most common types of amblyopia, strabismic and anisometropic, which are believed to have different neural bases. Several prominent theories of the neural basis of amblyopia will be directly investigated. We plan psychophysical and physiological experiments to test the ideas that amblyopia is a consequence of: abnormal development of local and long-range spatial interactions, reduced representation of the affected eye's activity in the brain, disarray of the affected eye's connections in the brain, and reduced visual efficiency (poor signal/noise processing) in central visual mechanisms. Psychophysical investigations focus on two specific areas: the degree of spatial interaction in amblyopia as a function of task type (contrast processing versus spatial precision or crowding), and the nature of reduced efficiency in form and motion processing. We will study the degree to which the visual deficits are first-order (at the level of the primary filters) or second-order (at a later stage of processing after integration and pooling of information from the first stage), and whether the second-order deficiencies are confined to spatial processing (form based) or include temporal processing deficits (motion based) as well. Physiological investigations are designed to directly test the hypotheses for the neural basis of amblyopia listed above. We will examine the possible substrates for abnormal spatial interaction and disarray in V1 neurons, look for correlates of second-order deficits and crowding in V2, and look for the site of reduced efficiency in extrastriate form and motion areas, MT and (presumably) V4. We will also look for evidence that binocularity is a deterministic factor for classes of amblyopia, and begin to investigate treatment strategies for preserving binocularity. ? ?
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