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NMDA媒介による酸化窒素の放出による長期的な増強の抑制

Y Izumi¹, D B Clifford, C F Zorumski

¹Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110.

Science (New York, N.Y.)

|August 28, 1992

まとめ

酸化窒素 (NO) の放出タイミングは,海馬の長期増強 (LTP) に影響を及ぼします. NOは,以前のN-メチル-D-アスパルテート (NMDA) 受容体活性と刺激性アミノ酸レベルに応じて,LTPを阻害または促進することができます.

科学分野:

神経科学は神経科学である.
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,
分子生物学は分子生物学である.

背景:

長期増強 (LTP) は,学習と記憶の重要なメカニズムです.
N-メチル-D-アスパルテート (NMDA) 受容体活性化はシナプス可塑性において重要な役割を果たします.
酸化窒素 (NO) は,シナプス調節を含む様々な神経機能に関与しています.

研究の目的:

ヒポキャンパスにおける長期増強 (LTP) の調節における酸化窒素 (NO) の役割を調査する.
NMDA受容体の活性化がLTPに対するNOの効果にどのように影響するかを決定する.
CA1シナプス増強に対するNOのタイミングに依存する効果を明らかにする.

主な方法:

海馬のCA1領域におけるシナプス反応の電気生理学的記録.
NMDA受容体アゴニスト/アンタゴニストを用いた薬理学的操作.
NO阻害剤 (L-NG-モノメチル-アルギニン,ヘモグロビン) とNOドナー (ナトリウムニトロプルシド) の適用.

主要な成果:

前テタニックのNMDA受容体活性化は,ヒッポキャンパスのLTPをブロックした.
このNMDA媒介のLTP抑制は,NO阻害剤によって逆転した.
ナトリウムニトロプロシドでNOの放出を模倣することで,LTPに対する抑制効果が再現されました.

結論:

シナプス活性に対するNO放出のタイミングは,LTP生成に極めて重要です.
NOは,LTPにおけるポジティブとネガティブの両方の調節作用を行なうことができます.
前回のNMDA受容体活性化と刺激性アミノ酸レベルは,海馬のLTPにおけるNOの調節機能に影響を与えます.

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