Cross-Modal Reinstatement of Thalamocortical Plasticity Accelerates Ocular Dominance Plasticity in Adult Mice

Abstract

Summary: Plasticity of thalamocortical (TC) synapses is robust during early development and becomes limited in the adult brain. We previously reported that a short duration of deafening strengthens TC synapses in the primary visual cortex (V1) of adult mice. Here, we demonstrate that deafening restores NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) of TC synapses onto principal neurons in V1 layer 4 (L4), which is accompanied by an increase in NMDAR function. In contrast, deafening did not recover long-term depression (LTD) at TC synapses. Potentiation of TC synapses by deafening is absent in parvalbumin-positive (PV+) interneurons, resulting in an increase in feedforward excitation to inhibition (E/I) ratio. Furthermore, we found that a brief duration of deafening adult mice recovers rapid ocular dominance plasticity (ODP) mainly by accelerating potentiation of the open-eye responses. Our results suggest that cross-modal sensory deprivation promotes adult cortical plasticity by specifically recovering TC-LTP and increasing the E/I ratio. : Plasticity of thalamocortical (TC) synapses is limited in adults. Rodríguez et al. demonstrate that a brief period of deafening adults recovers LTP at TC synapses in visual cortex and accelerates ocular dominance plasticity. These results suggest that cross-modal sensory deprivation may be an effective way to promote adult cortical plasticity. Keywords: cross-modal plasticity, thalamocortical LTP, visual cortex, adult cortical plasticity, E/I ratio, NMDA receptor function