Abstract Amblyopia (‘lazy eye’) is a neuro-development disorder of the visual cortex that occurs early in life and affects about 3% of the population worldwide. Amblyopia is associated with reduced visual acuity and contrast sensitivity in the non-dominant eye. In addition, the majority of individuals with amblyopia do not have measurable stereopsis or the ability to perceive depth from binocular information, which negatively impacts many tasks of daily life including eye-hand coordination and navigation. While studies have shown that about 25% of the amblyopic population does have residual stereopsis, the retinal locus that mediates this function is unknown. This proposal tests the hypothesis that when stereopsis is present in amblyopia, it is the periphery and not the central visual field that mediates depth perception. The first aim uses a novel procedure to map stereopsis in both central and peripheral locations to determine whether residual stereopsis is in fact mediated by the periphery. Our pilot data suggest that it is the periphery that mediates stereopsis in amblyopia. We will also determine whether this peripheral stereopsis accounts for fusional vergence, the movement of the two eyes to fuse monocular images to form a binocular percept. The second aim examines the relation between residual stereopsis and the documented suppression of the non-dominant eye under conditions of binocular viewing. We will measure the suppression zone for each individual and relate it to the zone of stereo-deficiency measured for that same individual. This within-participant comparison is essential to understanding the relation between suppression and stereo-deficiency in this special group of amblyopic individuals who have residual stereopsis. This group comprises about 50% of those with anisometropia (unequal refractive error), and about 10-40% of those with strabismus (eye deviation). This study will characterize each observer’s capacity for stereopsis across the visual field including the periphery, which has been ignored previously. The third aim will use electroencephalography (EEG) combined with a procedure to localize cortical source that produces the signals to understand the neural basis of suppression in individuals with and without stereopsis, and how well the non-dominant eye signal is represented on its own, and in the presence of a stimulus in the other eye, as well as how the two eyes’ signals are combined at different levels of the cortical hierarchy. If the peripheral visual field has a significant contribution to stereopsis in amblyopia, our study will establish the importance of clinically evaluating the potential for stereopsis in the periphery and for training peripheral locations to improve stereopsis.