グルタミン酸は,ドーパミンニューロンにおける阻害性ポストシナプス潜在性を媒介する
1Vollum Institute, Oregon Health Sciences University, Portland 97201, USA.
Nature
|July 17, 1998
まとめ
主要な脳神経伝達物質であるグルタミン酸は,ドーパミンニューロンにおけるメタボトロピク受容体 (mGluR1) を通して,抑制を特異的に媒介する. この発見は,グルタミン酸が単なる興奮剤であるという見解に異議を唱え,シナプス伝達におけるその二重の役割を明らかにした.
科学分野:
- 神経科学は神経科学である.
- 細胞生物学 細胞生物学
- 神経化学 神経化学とは
背景:
- ニューロン通信はグルタミン酸とGABAに依存し,イオノトロプ受容体経由で刺激と抑制を媒介する.
- グルタミン酸はまた,メタボトロピク受容体を活性化させ,第2伝達経路を通じてより遅い神経刺激を誘発します.
研究 の 目的:
- メタボトロピックグルタミン酸受容体 (mGluRs) によって媒介される新しい阻害性ポストシナプスポテンシャル (IPSP) を調査する.
- 腹中中脳ドーパミンニューロンにおけるmGluR媒介阻害の背後にあるメカニズムを解明する.
主な方法:
- ドーパミンニューロンにおけるメタボトロピックグルタミン酸受容体 (mGluR1) の活性化.
- 細胞内貯蔵物からカルシウムを動員する測定.
- アパミンに敏感なカリウム伝導性の変化の評価.
- ニューロン応答に対するアゴニスト被曝期間効果の分析.
主要な成果:
- mGluR1の活性化は,カフェイン/ライオノジンに敏感な貯蔵物からカルシウムを動員する.
- 以前に説明された遅いIPSPとは異なる,アパミンに敏感なユニークなカリウム伝導性が特定されました.
- 短期的なmGluR1の活性化により,ハイパーポラライゼーションが誘発され,長期間の適用により,無感化と脱ポラライゼーションが発生した.
結論:
- メタボトロピックグルタミン酸受容体 (mGluR1) は,ドーパミンニューロンにおける新しい形態のシナプス阻害を媒介する.
- シナプスで放出されるグルタミン酸は,抑制に続く急速な興奮を誘発し,二重の役割を果たすことを示します.
- シナプス伝達におけるグルタミン酸の機能は,これまで理解されていたよりも複雑で,刺激作用と抑制作用の両方を含む.
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