関節炎ラット脊髄後角におけるグリア依存性神経興奮増強

  • 池田 弘
    福井大学大学院工学研究科知能システム工学専攻, 福井大学生命科学複合研究教育センター
  • 西 良介
    福井大学大学院工学研究科知能システム工学専攻, 福井大学生命科学複合研究教育センター
  • 村瀬 一之
    福井大学大学院工学研究科知能システム工学専攻, 福井大学生命科学複合研究教育センター

書誌事項

タイトル別名
  • <b>Glia-mediated facilitation of neuronal excitation in the spinal dorsal horn in arthritic rats </b>

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   Sensitization in the spinal dorsal horn is believed to be a cellular mechanism for enhanced pain sensitivity. In this study, by using optical imaging with voltage-sensitive dye, we measured the neuronal excitation in spinal cord slices from normal rats and Complete Freund's Adjuvant (CFA)-induced arthritis rats. The amplitude of evoked-neuronal excitation in the substantia gelatinosa of arthritis rats was larger than normal rats and inhibited in the presence of a glial TCA cycle inhibitor, monofluoro-acetic acid. A gap-junction blocker, carbenoxolone inhibited neuronal excitation in arthritis rats one hour, but not one day after injection of CFA. In contrast, a microglial inhibitor minocycline, as well as P2Y receptor antagonsist reactive blue,inhibited neuronal excitation in arthritis rats one day, but not one hour after injection. These results suggest that facilitation of neuronal excitation mediated by glial cells in the gelatinosa underlies the induction of mechanical hyperalgesia in arthritis rats, and that the functional changes in glial cells take place in early stage of the arthritis.

収録刊行物

  • PAIN RESEARCH

    PAIN RESEARCH 23 (3), 151-157, 2008

    日本疼痛学会

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