Postsynaptic insertion of AMPA receptor onto cortical pyramidal neurons in the anterior cingulate cortex after peripheral nerve injury

Tao Chen, Wen Wang, Yu Lin Dong, Ming Ming Zhang, Jian Wang, Kohei Koga, Yong Hui Liao, Jin Lian Li, Timotheus Budisantoso, Ryuichi Shigemoto, Makoto Itakura, Richard L. Huganir, Yun Qing Li, Min Zhuo

Research output: Contribution to journalArticlepeer-review

Abstract

Long-Term potentiation (LTP) is the key cellular mechanism for physiological learning and pathological chronic pain. Postsynaptic accumulation of AMPA receptor (AMPAR) GluA1 plays an important role for injury-related cortical LTP. However, there is no direct evidence for postsynaptic GluA1 insertion or accumulation after peripheral injury. Here we report nerve injury increased the postsynaptic expression of AMPAR GluA1 in pyramidal neurons in the layer V of the anterior cingulate cortex (ACC), including the corticospinal projecting neurons. Electrophysiological recordings show that potentiation of postsynaptic responses was reversed by Ca2+ permeable AMPAR antagonist NASPM. Finally, behavioral studies show that microinjection of NASPM into the ACC inhibited behavioral sensitization caused by nerve injury. Our findings provide direct evidence that peripheral nerve injury induces postsynaptic GluA1 accumulation in cingulate cortical neurons, and inhibits postsynaptic GluA1 accumulation which may serve as a novel target for treating neuropathic pain.

Original languageEnglish (US)
Article number76
JournalMolecular Brain
Volume7
Issue number1
DOIs
StatePublished - Oct 31 2014

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience

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