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A High-content Assay for Monitoring AMPA Receptor Trafficking
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AAA+ATPアゼトラーゼは,AMPA受容体依存のシナプス性可塑性と行動を調節する
Jianmin Zhang1, Yue Wang, Zhikai Chi
1Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Cell
|April 19, 2011
まとめ
AAA+ ATPaseトラーゼは,表面AMPA受容体 (AMPAR) の内部化を媒介することによって,表面AMPA受容体を調節する. トラゼの削除はAMPARの除去を阻害し,シナプス可塑性に影響を与え,学習と記憶の欠陥につながります.
科学分野:
- 神経科学は神経科学である.
- 分子生物学は分子生物学である.
- バイオケミストリー バイオケミストリー
背景:
- 長期増強 (LTP) と長期抑うつ (LTD) を含むシナプス可塑性は,学習と記憶に不可欠です.
- AMPA受容体 (AMPAR) の表面表現は,シナプス活性と可塑性の重要な調節因子である.
研究 の 目的:
- AMPAR表面発現の新種の分子調節体を特定し,特徴づけること.
- シナプス性可塑性および認知機能におけるAAA+ATPアゼトラーゼの役割を明らかにする.
主な方法:
- 神経細胞におけるトラーゼ機能の特徴.
- マウスにおけるトラーゼの遺伝的削除 (Thorase null).
- ミニチュア刺激性ポストシナプス電流 (mEPSCs) の電気生理学的記録.
- トラセスのゼロマウスにおけるLTPとLTDの評価.
- 学習と記憶の欠陥に対する行動テスト.
主要な成果:
- トラーゼ (AAA+ ATPase) は,表面AMPAR発現の調節体として特定されました.
- トラーゼは,AMPAR-GRIP1複合体のATPアゼ依存分解を介してAMPARの内部化を媒介する.
- トラーゼの遺伝子削除により,AMPARの内部化が著しく減少しました.
- トラゼゼロマウスは,mEPSCの振幅が増加し,LTPが強化され,LTDが廃止された.
- トラゼゼロマウスは,学習と記憶に重大な欠陥を示した.
結論:
- トラーゼは,受容体の内部化を介してAMPAR表面発現を調節する上で重要な役割を果たします.
- トラーゼ機能の障害は,異常なシナプス可塑性,学習障害,記憶障害を引き起こす.
- トラーゼは,認知障害を理解し,潜在的に治療するための新しい分子標的を表しています.
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