ヒポキャンパスの内ニューロンにおける長期的なうつ病:シナプス前およびシナプス後イベントの共同要件
F Laezza1, J J Doherty, R Dingledine
1Neuroscience Graduate Program, Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Science (New York, N.Y.)
|August 28, 1999
まとめ
長期うつ病 (LTD) は海馬内ニューロンで発生し,以前の仮定に異議を唱える. このシナプス性可塑性は,AMPA受容体およびシナプス前mGluR7型受容体経由のカルシウム流入に依存しています.
科学分野:
- 神経科学は神経科学である.
- シナプスの可塑性
- ヒッポキャンパスの内ニューロン
背景:
- 長期うつ病 (LTD) は,主要なニューロンにおけるシナプス可塑性の重要な形態である.
- インターニューロンにおけるLTDの発生は,依然として議論の対象となっている.
研究 の 目的:
- CA3ヒポキャンパスの内ニューロンに LTD.が表れているかどうかを調査する.
- これらの内ニューロンにおけるLTDの基礎となる分子機構を解明する.
主な方法:
- 内ニューロンへのCA3刺激インプットのテタニック刺激.
- シナプスの強さを評価するための電気生理学的記録.
- 受容体の関与を調査するための薬理学的操作.
主要な成果:
- CA3ヒポキャンパスの内ニューロンでCa2+透過性AMPA受容体を発現していることが,LTD.で実証されました.
- LTDは,N-メチル-D-アスパルテート (NMDA) 受容体とは無関係でした.
- LTDには,AMPA受容体を通じたポストシナプスCa2+の流入と,プレシナプスmGluR7型受容体活性化が必要でした.
結論:
- 内ニューロンは,シナプス強さのプラスチックの変化を起こすことができる.
- 内ニューロンにおけるシナプス可塑性は,シナプス前後のグルタミン酸受容体の調整された作用を伴う.
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