アドレナリンα<sub>2</sub>作動薬全身投与による脊髄α<sub>1</sub>受容体を介した抑制性シナプス伝達の促進

DOI Web Site 被引用文献1件 参考文献32件 オープンアクセス
  • 舟井 優介
    自然科学研究機構 生理学研究所 神経シグナル研究部門 大阪市立大学大学院 医学研究科 麻酔科学
  • 西川 精宣
    大阪市立大学大学院 医学研究科 麻酔科学
  • 森 隆
    大阪市立大学大学院 医学研究科 麻酔科学
  • 浅田 章
    大阪市立大学大学院 医学研究科 麻酔科学
  • 井本 敬二
    自然科学研究機構 生理学研究所 神経シグナル研究部門 総合研究大学院大学 生理科学
  • 古江 秀昌
    自然科学研究機構 生理学研究所 神経シグナル研究部門 総合研究大学院大学 生理科学

書誌事項

タイトル別名
  • <b>Systemic α<sub>2</sub> agonist administration facilitates inhibitory synaptic transmission in the rat spinal dorsal horn </b><b>mediated through α</b><b><sub>1 </sub></b><b>adorenoceptors </b>

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説明

α2 adrenoceptors are widely distributed in the central nervous system and involved in various physiological functions such as analgesia, hypnosis, amnesia and circulation. α2 agonists generally used as sedative agents, are also known to have analgesic properties. Previous in vitro studies have shown detailed cellular actions of α2 agonists by using electrophysiological analyses. In the locus coeruleus (LC) of the brain stem, α2 agonists are thought to inhibit LC neuronal activity to exert their sedative actions. In the spinal cord, dexmedetomidine (DEX), a highly selective α2 agonist, directly hyperpolarized substantia gelatinosa (SG, lamina II of the spinal cord) neurons by activating α2A and α2C adrenoceptors. Little is known, however, how systemically administered α2 agonists modulates noxious transmission at the synaptic level in vivo. We made in vivo whole-cell patch-clamp record­ings from SG neurons in adult anesthetized rats and examined analgesic action of systemically administered DEX. Contrary to our expection, intravenous administration of DEX at doses of sedative range did not induced any hyperpolarization in all SG neurons tested. Interestingly, DEX at doses below sedative range dramatically enhanced spontaneous inhibito­ry postsynaptic currents (IPSCs) in most of SG neurons tested. This facilitatory action of DEX was completely disappeared in spinalized rats, and spinal application of prazosin, an α1 antagonist, inhibited the facilitation of spinal IPSCs by DEX. These results suggest that systemically administered DEX at doses below sedative range paradoxically enhances descending noradrener­gic inhibitory pathway and results in facilitation of inhibitory synaptic transmission in the spinal dorsal horn. Our findings provide a new insight into the usefulness of α2 agonists for therapeutic intervention against acute and chronic pain.

収録刊行物

  • PAIN RESEARCH

    PAIN RESEARCH 28 (3), 145-153, 2013

    日本疼痛学会

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