シナプス端末の内部カルシウムの値上昇により,エンドサイトーシスが抑制される
1Department of Neurobiology and Behavior, State University of New York, Stony Brook, 11794-5230.
Nature
|August 25, 1994
まとめ
細胞内カルシウム ([Ca2+]i) の値が上昇すると,神経伝達物質のリサイクルにおける重要なステップであるシナプス膀内細胞化を阻害する. このカルシウムに依存するフィードバックメカニズムは,シナプス活動とうつ病を調節する可能性があります.
科学分野:
- 神経科学は神経科学である.
- 細胞生物学 細胞生物学
- シナプス性可塑性 (Synaptic Plasticity) とは,シナプス性可塑性 (Synaptic Plasticity) とは,シナプス性可塑性 (Synaptic Plasticity) とは,シナプス性可塑性 (Synaptic Plasticity) とは,シナプス性可塑性 (Synaptic Plasticity) とは,シナプス性可塑性 (Synaptic Plasticity) とは,シナプス性 (Synaptic Plasticity) とは,シナプス性 (Synaptic Plasticity) とは,シナプス性 (Synaptic Plasticity) とは,シナプス性 (Synaptic Plasticity) とは,シナプス性 (Synaptic Plasticity) とは,シナプス性 (Synaptic) とは,
背景:
- シナプス伝播は,膀のエクソサイトーシスとエンドサイトーシスを含む.
- エンドサイトーシスによる膜回収は,膀のリサイクルに不可欠です.
- エクソサイトーシスはカルシウム依存性であることが知られている.
研究 の 目的:
- 細胞内カルシウム濃度 ([Ca2+]i) がシナプス胞内細胞を調節する役割を調査する.
- カルシウムがエクソサイトーシス後の膜回収率に影響するかどうかを判断する.
主な方法:
- 網膜双極性ニューロンのシナプス端末の容量測定.
- 細胞内カルシウムのレベルを操作して,内細胞症への影響を評価する.
主要な成果:
- エンドოციトーシスは,上昇した[Ca2+]iによって有意に抑制された.
- 膜回収の速度は[Ca2+]i (ヒル係数4) に大きく依存していた.
- [Ca2+]i >= 900 nMでエンドサイトーシスが完全に廃止されました.
結論:
- 細胞内カルシウムは,内細胞症のネガティブなフィードバックの調節剤として作用する.
- このカルシウム媒介のフィードバックは,神経伝達物質の分泌後の膜の回復を制御する.
- このメカニズムは,膀のリサイクルに影響することによって,活動に依存したシナプス抑うつに寄与する可能性があります.
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