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

Cell Rep. 2018 Sep 25;24(13):3433-3440.e4. doi: 10.1016/j.celrep.2018.08.072.


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.

Keywords: E/I ratio; NMDA receptor function; adult cortical plasticity; cross-modal plasticity; thalamocortical LTP; visual cortex.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Auditory Perception*
  • Excitatory Postsynaptic Potentials
  • Female
  • Inhibitory Postsynaptic Potentials
  • Interneurons / metabolism
  • Interneurons / physiology
  • Long-Term Potentiation*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Sensory Deprivation
  • Thalamus / cytology
  • Thalamus / physiology*
  • Visual Cortex / cytology
  • Visual Cortex / physiology*
  • Visual Perception*


  • Receptors, N-Methyl-D-Aspartate