Aplysiaにおける長期的なヘテロシナプス阻害

P G Montarolo¹, E R Kandel, S Schacher

¹Howard Hughes Medical Institute, Columbia University, College of Physicians and Surgeons, New York, New York.

Nature

|May 12, 1988

まとめ

ペプチドフェメトアルグフェアミド (FMRFamide) は,アプリシアの長期シナプス低下を誘発する.

科学分野:

神経科学は神経科学である.
細胞神経科学は細胞神経科学である.
シナプスの可塑性

背景:

アプリシアのの引き出し反射におけるシナプス伝達は,短期的および長期的調節を示す.
数分続く短期間のシナプス抑うつは,アラキドン酸リポキシゲネーゼ経路経由でフェメトアルグフェアミド (FMRFamide) によって誘発される.

研究の目的:

アプリシアのの退去レフレクスの長期シナプス抑うつ (LTD) の誘導を調査する.
FMRFamideがLTDを誘発できるかどうかを判断し,短期的なうつ病および他の調節経路との特徴を比較する.

主な方法:

モノシナプス感覚と運動のつながりを研究するために,アプリシア細胞培養を用いた.
FMRFamideを2時間以上繰り返し投与すると,長期的な変化が起こります.
タンパク質合成阻害剤であるアニソマイシンのFMRFamide誘発性うつ病に対する効果を調査した.

主要な成果:

FMRFamideを2時間以上5回投与すると,24時間続く長期のシナプス低下が誘発された.
FMRFamideによって誘発されたLTDは送信機特異的であり,ドーパミンおよび低周波刺激はLTDを誘発しなかった.
長期的なうつ病は,短期的なうつ病とは異なり,アニソマイシンによって阻害され,タンパク質合成の必要性を示しました.

結論:

Aplysiaにおける長期のシナプス抑制は,長期の促進と同様に,タンパク質合成を必要とします.
ヘテロシナプス性うつ病は,ファシリテーションと同様に,短期的および長期的形態の両方で存在し,後者は遺伝子製品に依存しています.

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