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

被引：0

作者：

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

机构：

[1] Frontier Institute of Science and Technology,Center for Neuron and Disease

[2] Xi'an Jiaotong University,Department of Anatomy

[3] Histology and Embryology and K.K. Leung Brain Research Center,Department of Physiology, Faculty of Medicine

[4] the Fourth Military Medical University,Division of Cerebral Structure

[5] Center for the Study of Pain,Department of Biochemistry

[6] University of Toronto,Department of Neuroscience and Howard Hughes Medical Institute

[7] National Institute for Physiological Sciences,undefined

[8] Kitasato University School of Medicine,undefined

[9] Johns Hopkins University School of Medicine,undefined

来源：

Molecular Brain | / 7卷

关键词：

Nerve Injury; Anterior Cingulate Cortex; Long Term Potentiation; Mechanical Hyperalgesia; Rostral Ventromedial Medulla;

D O I：

暂无

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学科分类号：

摘要：

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.

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