• J. Neurosci. · Apr 2014

    Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity.

    • Nian Gong, Qi Xiao, Bin Zhu, Chang-Yue Zhang, Yan-Chao Wang, Hui Fan, Ai-Niu Ma, and Yong-Xiang Wang.
    • King's Laboratory, Shanghai Jiao Tong University School of Pharmacy, Shanghai 200240, China.
    • J. Neurosci. 2014 Apr 9;34(15):5322-34.

    AbstractThis study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states.

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