海馬の単一回路における抑制から刺激への周波数依存のスイッチ
Masahiro Mori1, Mathias H Abegg, Beat H Gähwiler
1Brain Research Institute, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland. mori@hifo.unizh.ch
Nature
|September 24, 2004
まとめ
ヒポキャンパスのモス繊維は,非シナプス経路を通じてCA3ピラミッド細胞を阻害することができます. この阻害信号は,発射頻度が増加すると興奮に切り替え,情報処理のための新しいシナプス機構を明らかにします.
科学分野:
- 神経科学は神経科学である.
- シナプスの可塑性
- 計算神経科学とは
背景:
- ヒポキャンプスは,記憶と認知に不可欠です.
- 伝統的に三シナプス刺激回路として見られている.
- CA3へのモッシーファイバーの入力は,三シナプス経路の鍵です.
研究 の 目的:
- CA3ピラミッド細胞へのモッシーファイバーのインプットの役割を調査する.
- モッシー繊維が刺激または阻害を媒介するかどうかを判断する.
- シナプス応答の極性に対する発射周波数の影響を調べる.
主な方法:
- ネズミの腸内海馬切片培養で接続された細胞ペアから記録.
- 単一作用電位を,歯状粒子の細胞に呼び起こします.
- CA3ピラミッド細胞におけるシナプス反応の分析.
主要な成果:
- 歯状粒細胞の単一作用電位は,CA3ピラミッド細胞の純抑制を誘発する.
- ディシナプス的なフィードフォワード阻害はモノシナプス刺激を覆す.
- プレシナプス発射頻度の増加は,抑制から刺激への応答を切り替えます.
結論:
- モッシー繊維の入力は,抑制と刺激の両方を媒介することができます.
- シナプス反応の極性スイッチは,シナプス前発射周波数に基づいています.
- このダイナミックなスイッチングは,ヒポカンパの情報処理に不可欠な新しいシナプスメカニズムです.
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