素早い神経伝達物質の放出は,AMPA型グルタミン酸受容体を通してCaの流入によって引き起こされます
Andrés E Chávez1, Joshua H Singer, Jeffrey S Diamond
1Synaptic Physiology Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3701, USA.
Nature
|October 13, 2006
まとめ
網膜におけるフィードバック阻害は,新しいメカニズムに依存しています. A17アマクリン細胞からのGABAの放出は,電圧ゲートカルシウムチャネルではなく,カルシウム浸透性AMPA受容体によって誘発され,新しい神経回路の経路を明らかにします.
科学分野:
- 神経科学は神経科学である.
- 網膜生理学 網膜生理学とは
- シナプス伝送 シナプス伝送
背景:
- A17アマクリン細胞と棒双極細胞 (RBCs) の間の相互シナプスは,網膜の光誘発反応にとって極めて重要です.
- A17細胞から赤血球へのGABA (ガンマアミノバター酸) によって媒介されるフィードバックの抑制は,視覚的処理を形作る.
- A17細胞のデンドライトからGABAの放出を制御する正確なメカニズムは未確定のままでした.
研究 の 目的:
- A17アマクリン細胞からのGABA放出を制御する分子機構を解明する.
- 電圧誘導カルシウムチャネル (VGCC) がこれらのシナプスでGABAの放出を媒介するかどうかを調査する.
- フィードバック阻害に関与するカルシウム源とシグナル伝達経路を特定するために.
主な方法:
- ネズミの網膜スライスによる電気生理学的記録.
- 受容体とイオンチャネルの薬理学的操作.
- 細胞内カルシウム動態を監視するためのカルシウムイメージング技術.
主要な成果:
- A17細胞からのGABA放出は,VGCCsと膜脱極化とは独立しています.
- カルシウム浸透性AMPA受容体 (AMPARs) 経由によるカルシウムの流入はGABAの放出を誘発する.
- AMPAR媒介のカルシウムシグナリングは,内部貯蔵からカルシウム誘発カルシウム放出 (CICR) によって増幅されます.
結論:
- VGCCsから独立した新しい形の高速シナプス伝播が網膜で動作します.
- カルシウム浸透性AMPARおよびCICRは,A17アマクリンおよび赤血球回路におけるフィードバック抑制に不可欠です.
- この発見は,網膜のニューラル回路の活動を調節するための,以前は認識されなかったメカニズムを明らかにしています.
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