Abstract
Dark exposure initiated in adulthood reactivates robust ocular dominance plasticity in the visual cortex. Here, we show that a critical component of the response to dark exposure is the rejuvenation of inhibitory synaptic transmission, resulting in a decrease in functional inhibitory synaptic density, a decrease in paired-pulse depression, and a reexpression of endocannabinoid-dependent inhibitory long-term depression (iLTD). Importantly, pharmacological acceleration of the maturation of inhibition in dark-exposed adults inhibits the reexpression of iLTD and the reactivation of ocular dominance plasticity. Surprisingly, dark exposure initiated earlier in postnatal development does not rejuvenate inhibitory synaptic transmission or facilitate rapid ocular dominance plasticity, demonstrating the presence of a refractory period for the regulation of synaptic plasticity by visual deprivation.