脊髄内カンナビノイドとCB1受容体は,C繊維誘発のヘテロシナプス疼痛感受性を媒介する

Alejandro J Pernía-Andrade¹, Ako Kato, Robert Witschi

¹Institute of Pharmacology and Toxicology, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.

Science (New York, N.Y.)

|August 8, 2009

まとめ

強い感受性インプットは脊髄内分泌カナビノイドを誘発し,カンナビノイドCB1受容体を活性化します. これにより,脊髄の背中角の阻害が減り,中央の痛みに対する感受性が生じます.

科学分野:

神経科学は神経科学である.
痛みの研究痛みの研究
脊髄生理学脊髄生理学

背景:

脊髄の背中角のシナプス阻害の低下は,慢性的な痛みに寄与する.
既知の経路は,炎症性および神経疾患性疼痛状態を含む.
セントラル・ハイパーアルゲシアは,炎症や神経病に伴わずに起こり,強烈な神経感受的入力によって引き起こされます.

研究の目的:

強烈な知覚の入力によって引き起こされる中心的ハイパーアルゲージアのメカニズムを調査する.
この過程におけるエンドカンナビノイドとカンナビノイド受容体の役割を特定する.
背中角の痛みを制御する回路へのそれらの貢献を理解する.

主な方法:

脊髄の背中角が,激しい感覚刺激に与える反応に焦点を当てたものです.
エンドカンナビノイドと1型カンナビノイド (CB1) 受容体の役割を調べました.
GABAやグリシンなどの阻害性神経伝達物質のシナプス発散への影響を調査した.

主要な成果:

強い神経受容刺激により,脊髄の背中角でエンドカンナビノイドが生成されます.
エンドカンナビノイドは,阻害性背中角ニューロン上のCB1受容体を活性化させます.
この活性化はGABAとグリシン放出を減少させ,シナプス阻害を減少させます.
ノシセプティブニューロンは,痛みのない刺激によって興奮し,感受性を示します.

結論:

脊髄内カンナビノイドとCB1受容体は,ヘテロシナプス疼痛感受性を媒介する.
背中角の痛みを制御する回路に予期せぬ役割を果たします.
これらの発見は,特定のタイプの慢性疼痛の管理のための潜在的なターゲットを提供します.

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