Temporary retinal inactivation reverses effects of long-term monocular deprivation in visual cortex by induction of burst mode firing in the thalamus.

Monocular deprivation during an early postnatal critical period causes amblyopia, an impairment of vision in one eye, by altering the development of synapses in the primary visual cortex (V1). Prior studies have shown that these synaptic changes can be rapidly reversed after the critical period by temporarily inactivating the non-deprived (fellow) eye with tetrodotoxin (TTX). Here, we show in mice that the inactivation of one eye causes dorsal lateral geniculate nucleus (dLGN) neurons postsynaptic to the other eye to fire in high-frequency bursts due to recruitment of the low-threshold voltage-gated calcium channels. Elimination of bursting by genetic deletion of CaV3.1 in the dLGN prevents the therapeutic effect of retinal inactivation without affecting another prominent form of experience-dependent synaptic modification. Inactivation of the amblyopic eye alone also triggered full recovery, suggesting that dLGN bursting is both necessary and sufficient to restore synaptic strength in the visual cortex after retinal silencing.