Abstract
Enduring amblyopia after early imbalanced binocular input is a classic example of critical period biology across species. Recovery of visual acuity is typically poor in adulthood due to both the extensive loss of connections and declining neuroplasticity in primary sensory areas. The discovery that rewiring is actively limited in adulthood rather than passively lost with age inspires novel therapeutic approaches to lift such brakes on plasticity. Notably, these mechanisms converge on pivotal inhibitory circuits in primary visual cortex. This talk will overview insights from rodent models of acuity recovery which may augment that of humans endowed with higher visual areas exhibiting prolonged plasticity.