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

Cell Rep

Mind/Brain Institute, Department of Neuroscience, Johns Hopkins University, 3400 N. Charles Street, Dunning Hall, Baltimore, MD 21218, USA; Cellular Molecular Developmental Biology and Biophysics Program, Johns Hopkins University, Mudd Hall, 3400 N. Charles Street, Baltimore, MD 21218, USA. Electronic address:

Published: September 2018

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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233297PMC
http://dx.doi.org/10.1016/j.celrep.2018.08.072DOI Listing

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