脊髄内痛覚伝達におけるGABA<sub>B</sub>受容体の役割

DOI Web Site 参考文献32件
  • 竹島 香
    九州大学大学院医学研究院 統合生理学
  • 古江 秀昌
    九州大学大学院医学研究院 統合生理学
  • 吉村 恵
    九州大学大学院医学研究院 統合生理学

書誌事項

タイトル別名
  • <b>The role of GABA<sub>B</sub> receptor in spinal nociceptive transmission</b>

この論文をさがす

抄録

   Gamma-aminobutyric acid (GABA) is one of the important inhibitory neurotransmitters in the central nervous system. GABA acts on GABA receptors classified into metabotropic G-proteincoupled GABAB receptor and ionotropic GABAA receptor. In the substantia gelatinosa (SG) of the spinal dorsal horn, noxious information is transmitted through Aδ and C afferent fibers. In addition to the excitatory synaptic inputs from the noxious afferent fibers, SG neurons also receive abundant GABAergic synaptic inputs from spinal interneurons. Therefore, the SG is thought to have a critical role for GABA-mediated modulation of nociceptive transmission. In behavioral studies, intrathecal administration of baclofen, a selective GABAB receptor agonist, produces antinociception. In order to determine the cellular mechanisms of GABAB receptor-mediated modulation of spinal nociceptive transmission, we examined actions of baclofen on excitatory synaptic transmission in the SG using whole-cell patch-clamp recordings from spinal cord slices and in vivo preparations of rats. SG neurons in the slices exhibited miniature excitatory postsynaptic currents (mEPSCs) in the presence of TTX. Baclofen decreased the frequency but not amplitude of mEPSCs. Stimulation of the dorsal root attached to the slices evoked monosynaptic EPSCs in SG neurons mediated through activation of Aδ and C afferent fibers. Baclofen more potently inhibited the amplitude of C fiber-evoked EPSCs than that of Aδ fiber-evoked EPSCs. In the in vivo patch-clamp analysis, baclofen applied to the surface of the spinal cord, suppressed the amplitude of EPSCs in SG neurons evoked by pinch stimulation applied to the skin. Baclofen also induced outward currents which were blocked by GDP-β-S or Cs+ added to the patch pipette solution. These results suggest that baclofen acts on presynaptic terminals of mechano-sensitive C and Aδ afferent fibers in the SG to reduce glutamate releases and on the postsynaptic membrane to induce membrane hyperpolarization by activation of K+ channels. Our findings provide a cellular explanation for the GABAB receptor-mediated antinociception in the spinal cord.

収録刊行物

  • PAIN RESEARCH

    PAIN RESEARCH 22 (1), 1-9, 2007

    日本疼痛学会

参考文献 (32)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ