単純なニューラルネットワークにおける活動に依存したシナプス低下の拡散

R M Fitzsimonds¹, H J Song, M M Poo

¹Department of Biology, University of California at San Diego, La Jolla 92093-0357, USA.

Nature

|July 31, 1997

まとめ

グルタマタージックシナプスのシナプス抑制は,活性化された接続を超えて広がります. この神経ネットワークの可塑性は,シナプス前とシナプス後の入力に影響しますが,出力には影響しません.

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:

長期うつ病 (LTD) はシナプス可塑性の重要なメカニズムである.
シナプス変異の広がりを理解することは,ニューラルネットワークの機能を理解するために不可欠です.

研究の目的:

養殖ヒポカンパの神経ネットワークにおける活動誘発シナプス低下の伝播パターンを調査する.
シナプス変異が活性化されたシナプスに限られているか,ネットワーク内で広がっているかを判断する.

主な方法:

培養された海馬の神経細胞に,三重の全細胞記録が行われました.
長期的うつ病は,グルタマタージックシナプスで誘発された.

主要な成果:

グルタマタージックシナプスでLTDを誘導すると,うつ病はプレシナプスインプットに逆行して拡散する.
うつ病は,プレシナプスニューロンの他の出力とポストシナプスニューロンの収束インプットに横方向に広がります.
ポストシナプスニューロンの出力では前向きの伝播が観察されず,GABAergic LTD.ではプレシナプス伝播は発生しませんでした.

結論:

アクティビティ誘発のシナプス改変は,当初活性化されたシナプスに限定されない.
シナプス性うつ病は,神経ネットワーク全体に選択的に広がり,複数の接続に影響を与えます.
これらの発見は,これまで理解されていたよりも,シナプス性可塑性の範囲がより広いことを明らかにしています.

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