Recovery from chronic monocular deprivation following reactivation of thalamocortical plasticity by dark exposure.

Abstract

Chronic monocular deprivation induces severe amblyopia that is resistant to spontaneous reversal. However, dark exposure initiated in adulthood reactivates synaptic plasticity in the visual cortex and promotes recovery from chronic monocular deprivation in Long Evans rats. Here we show that chronic monocular deprivation induces a significant decrease in the density of dendritic spines on principal neurons throughout the deprived visual cortex. Nevertheless, dark exposure followed by reverse deprivation promotes the recovery of dendritic spine density of neurons in all laminae. Importantly, the ocular dominance of neurons in thalamo-recipient laminae of the cortex, and the amplitude of the thalamocortical visually evoked potential recover following dark exposure and reverse deprivation. Thus, dark exposure reactivates widespread synaptic plasticity in the adult visual cortex, including thalamocortical synapses, during the recovery from chronic monocular deprivation.