| First Author | Rodríguez G | Year | 2018 |
| Journal | Cell Rep | Volume | 24 |
| Issue | 13 | Pages | 3433-3440.e4 |
| PubMed ID | 30257205 | Mgi Jnum | J:267845 |
| Mgi Id | MGI:6269295 | Doi | 10.1016/j.celrep.2018.08.072 |
| Citation | Rodriguez G, et al. (2018) Cross-Modal Reinstatement of Thalamocortical Plasticity Accelerates Ocular Dominance Plasticity in Adult Mice. Cell Rep 24(13):3433-3440.e4 |
| abstractText | 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. |
