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Postsynaptic insertion of AMPA receptor onto cortical pyramidal neurons in the anterior cingulate cortex after peripheral nerve injury
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  • 作者:Tao Chen (1) (2) (3)
    Wen Wang (2)
    Yu-Lin Dong (2)
    Ming-Ming Zhang (2)
    Jian Wang (2)
    Kohei Koga (1) (3)
    Yong-Hui Liao (2)
    Jin-Lian Li (2)
    Timotheus Budisantoso (4)
    Ryuichi Shigemoto (4)
    Makoto Itakura (5)
    Richard L Huganir (6)
    Yun-Qing Li (2)
    Min Zhuo (1) (3)

    1. Center for Neuron and Disease
    ; Frontier Institute of Science and Technology ; Xi鈥檃n Jiaotong University ; Xi鈥檃n ; China
    2. Department of Anatomy
    ; Histology and Embryology and K.K. Leung Brain Research Center ; the Fourth Military Medical University ; Xi鈥檃n ; 710032 ; China
    3. Department of Physiology
    ; Faculty of Medicine ; Center for the Study of Pain ; University of Toronto ; 1 King鈥檚 College Circle ; Toronto ; Ontario ; M5S 1A8 ; Canada
    4. Division of Cerebral Structure
    ; National Institute for Physiological Sciences ; Myodaiji ; Okazaki ; 444-8787 ; Japan
    5. Department of Biochemistry
    ; Kitasato University School of Medicine ; Sagamihara ; Kanagawa ; Japan
    6. Department of Neuroscience and Howard Hughes Medical Institute
    ; Johns Hopkins University School of Medicine ; Baltimore ; MD ; USA
  • 刊名:Molecular Brain
  • 出版年:2014
  • 出版时间:December 2014
  • 年:2014
  • 卷:7
  • 期:1
  • 全文大小:3,434 KB
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  • 刊物主题:Neurosciences; Neurology;
  • 出版者:BioMed Central
  • ISSN:1756-6606
文摘
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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