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Abstract: Recent studies in adult humans have shown that short-term deprivation of one eye (1-3hrs) dramatically shifts the balance in favor of this eye for over an hour afterwards. This surprising result runs counter to the classical understanding of both the limits of adult cortical plasticity as well as the Hebbian nature of monocular deprivation. The STMD paradigm, then, has uncovered a poorly understood yet important feature of early binocular integration. We have confirmed this striking observation in initial functional imaging studies of primate visual cortex, thereby also showing a cortical locus. As pattern deprivation also elicits this non-Hebbian STMD effect and its recovery behavior is dependent on binocular interactions, the underlying neural mechanisms cannot be retinal in origin. In addition, multi-electrode recordings have begun to characterize the neural mechanisms by which interocular balance in cortex is achieved and perturbed by STMD. Identification of the classes of neurons and circuits involved, their location in the visual pathways and their contribution to STMD and binocular integration will inform the refinement of a computational model. In turn, this critical knowledge will further guide clinically important therapies for amblyopia and other applications of adult cortical plasticity.