共通の分子経路は,シナプス刺激の長期的増強と遅いシナプス抑制を媒介する

Cindy Shen Huang¹, Song-Hai Shi, Jernej Ule

¹Howard Hughes Medical Institute and Departments of Physiology and Biochemistry, University of California, San Francisco, CA 94143, USA.

Cell

|October 11, 2005

まとめ

この研究は,同じ経路が刺激性および阻害性シナプス可塑性の両方を強化することを明らかにしています. しかし,Nova-2タンパク質は阻害性可塑性において極めて重要であり,学習と記憶に影響を及ぼします.

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
分子生物学は分子生物学である.

背景:

dendritic spinesのシナプス可塑性は,学習と記憶の基礎となっている.
刺激性ポストシナプス電流 (EPSCs) の長期増強 (LTP) はよく研究されています.
刺激性LTPにおける重要な役割は,NMDA受容体とCaMKIIである.

研究の目的:

阻害性ポストシナプス電流 (IPSCs) の可塑性を調査する.
抑制性可塑性におけるN-メチル-D-アスパラート受容体 (NMDA-R) とCa2+/カルモジュリン依存タンパク質キナーゼII (CaMKII) 経路の役割を調査する.
シナプス性可塑性におけるNova-2タンパク質の関与を決定する.

主な方法:

CA1ピラミッドニューロンにおける電気生理学的記録.
遅い阻害性ポストシナプス電流 (sIPSCs) のLTPを調査する.
Nova-2タンパク質が欠けているノックアウトマウスを利用した.

主要な成果:

NMDA-R/CaMKII経路は,GABA (((B)) 受容体とGIRKチャネルによって媒介されるsIPSCのLTPを誘導する.
sIPSCsのLTPは,EPSCではなく,Nova-2.2が欠けているマウスでは廃止されました.
Nova-2は,阻害性シナプス可塑性にとって不可欠である.

結論:

同じシグナル伝達経路は,刺激性および阻害性シナプス性可塑性の両方を調節する.
Nova-2は,刺激性可塑性における役割とは異なり,抑制性可塑性において重要な役割を果たします.
Nova-2の調節不良は,シナプス可塑性の低下に関連した神経学的障害に寄与する可能性があります.

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