前シナプスメタボトロピックグルタミン酸受容体のシグナル伝達におけるカルモジュリン依存性
V O'Connor1, O El Far, E Bofill-Cardona
1Department of Neurochemistry, Max Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany.
Science (New York, N.Y.)
|November 5, 1999
まとめ
前シナプスメタボトロピクグルタミン酸受容体 (mGluRs) は神経伝達を制御する. カルシウム-カルモジュリン結合はGタンパク質サブユニットを放出し,mGluRsが刺激性神経伝達を阻害することを可能にします.
科学分野:
- 神経科学は神経科学である.
- 分子生物学は分子生物学である.
- セルラー・シグナリング
背景:
- プレシナプスメタボトロピックグルタミン酸受容体 (mGluRs) はグルタミン酸性神経伝達を調節する.
- グループIIIのmGluRは,タンパク質の相互作用に関与する細胞内カルボキシル端尾を有する.
研究 の 目的:
- グループIIIのmGluRsがイオン電流と神経伝達を調節するメカニズムを解明する.
- mGluR機能におけるカルモジュリンとGタンパク質ベタガマサブユニットの役割を調査する.
主な方法:
- 変異を利用して,IIIグループ mGluRsのカルモジュリン結合部位を破壊する.
- カルモジュリン機能を抑制するためにカルモジュリン抗体を使用する.
- これらの操作がGタンパク質媒介によるイオン電流の調節と刺激性神経伝達に与える影響を評価する.
主要な成果:
- カルモジュリン結合とカルモジュリン抗体に影響する変異は,mGluR 7.によるイオン電流のGタンパク質媒介変調を阻害した.
- また,カルモジュリン抗薬は,プレシナプス的なmGluRsによって媒介される刺激性神経伝送の抑制を阻害した.
- これらの発見は,カルモジュリンとGタンパク質ベタガマサブユニットの相互排他的結合をmGluR C-tailに示す.
結論:
- Ca(2+) -カルモジュリンを含むプレシナプス調節のための新しいメカニズムが特定されました.
- Ca(2+) -カルモジュリンは,グループIIIのmGluRsからGタンパク質ベタガマサブユニットを放出するために不可欠です.
- この放出は,プレシナプス的なmGluRsを介してグルタマタージック自己抑制を媒介するために必要です.
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