Abstract
Our recent studies have demonstrated that the cortical circuitry supporting the monocular and binocular RF properties of V1 and V2 neurons in macaque monkeys is qualitatively adult like as early as 4 weeks of age, and, if not, by 8 weeks of age. However the functional organization of visual cortex in neonates and infants is fragile and needs ‘normal’ visual experience to complete its postnatal development. Experiencing binocular imbalance soon after birth disrupts this development and can result in binocular vision anomalies and often amblyopia. What happens to the visual brain of amblyopic subjects that experience early binocular imbalance is not well understood except for some aspects of early monocular form deprivation. This talk will present the results of studies in primate models of strabismic and anisometropic amblyopia, and make a proposal on how some of monocular deficits in amblyopes may develop. Our earlier studies established that binocular imbalance in infant monkeys immediately initiates interocular suppression in their visual cortex, which persists until adulthood. We also found that the depth of amblyopia in individual strabismic monkeys is highly correlated with the strength of binocular suppression in V1 and V2. I will present our preliminary data to demonstrate that such robust binocular suppression can disrupt the functional development of cortical circuits supporting the spatial map of subunits within the receptive field of a given V2 neuron in amblyopic monkeys, and also, suppression may affect the timing and reliability of spiking by these neurons.
Meeting abstract presented at VSS 2013