ラット脊髄スライスの膠様質ニューロンにおける興奮性および抑制性のシナプス伝達に及ぼすガラニンの作用

DOI Web Site 参考文献32件
  • 岳 海源
    佐賀大学医学部 生体構造機能学講座（神経生理学分野）
  • 藤田 亜美
    佐賀大学医学部 生体構造機能学講座（神経生理学分野）
  • 朴 蓮花
    佐賀大学医学部 生体構造機能学講座（神経生理学分野）
  • 青山 貴博
    佐賀大学医学部 生体構造機能学講座（神経生理学分野）
  • 上村 聡子
    佐賀大学医学部 生体構造機能学講座（神経生理学分野）
  • 中塚 映政
    佐賀大学医学部 生体構造機能学講座（神経生理学分野）
  • 熊本 栄一
    佐賀大学医学部 生体構造機能学講座（神経生理学分野）

書誌事項

タイトル別名
  • <b>Effect of galanin on excitatory and inhibitory synaptic </b><b>transmission in substantia gelatinosa neurons </b><b>of rat spinal cord slices </b>

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Galanin (Gal), a neuropeptide composed of 29 / 30 amino acid residues, is thought to play a pivotal role in various physiological functions including nociception. There is much evidence showing that Gal plays a role in modulating nociceptive transmission at the rat spinal cord level. Gal and three types (GalR1-3) of receptor for this are expressed in rat dorsal root ganglion neurons and spinal dorsal horn neurons. Behavioral studies have demonstrated that intrathecal administration of Gal modulates nociceptive transmission in rats. Cellular mechanisms for this Gal action, however, have not been fully examined yet. We have previously reported that Gal facilitates the spontaneous release of L-glutamate from nerve terminals by activating GalR2/R3 without a change in L-glutamate-receptor sensitivity and also produces a membrane hyperpolarization through GalR1 activation and/or depolarization in rat substantia gelatinosa (SG) neurons which play a crucial role in regulating nociceptive transmission through primary-afferent Aδ and C fibers from the periphery. In order to further know a role of Gal in regulating nociceptive transmission, in neurons where the postsynaptic response of Gal was not seen, we examined the action of Gal (0.1 µM) on dorsal root-evoked monosynaptic Aδ-fiber and C-fiber glutamatergic excitatory synaptic transmission, where the blind whole-cell patch-clamp technique was applied to SG neurons of an adult rat spinal cord slice attached with a dorsal root. Since SG neurons receive not only excitatory but also inhibitory inputs, the effect of Gal (0.1 µM) on inhibitory synaptic transmission was also examined. Gal reduced more effectively the peak amplitude of monosynaptic Aδ fiber than C-fiber excitatory postsynaptic current (EPSC) recorded at a holding potential of -70 mV; this was so in a neuron where both Aδ-fiber and C-fiber EPSCs were evoked. These Gal effects were mimicked by a selective GalR2/R3 agonist galanin (2-11) but not a GalR1 agonist M617. On the other hand, spontaneous and focally-evoked (GABAergic and glycinergic) inhibitory synaptic transmission was not affected by Gal (0.1 µM). These results indicate that Gal reduces the evoked release of L-glutamate onto SG neurons from primary-afferent Aδ-fiber and C-fiber central terminals, possibly by activating GalR2/R3. This Gal effect could contribute to its regulation of nociceptive transmission.

収録刊行物

  • PAIN RESEARCH

    PAIN RESEARCH 25 (3), 159-169, 2010

    日本疼痛学会

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