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NMDA受容体によるNMDA受容体によるNMDA受容体によるNMDA受容体によるNMDA受容体によるNMDA受容体によるP物質の放出に関するNMDA受容体によるNMDA受容体によるP物質の放出に関するNMDA受容体の調節
H Liu1, P W Mantyh, A I Basbaum
1Department of Anatomy, University of California San Francisco, 94143, USA.
Nature
|April 17, 1997
まとめ
脊髄におけるN-メチル-D-アスパルテート (NMDA) 受容体の活性化により,物質Pが放出され,持続的な痛みと構造的変化を引き起こす. 物質P受容体または経路をブロックすると,これらの効果が軽減され,新しい痛み治療のターゲットが示唆されます.
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
- 脊髄損傷による脊髄損傷
背景:
- 重度の損傷は,背部の角のニューロンの過興奮を引き起こし,慢性的な痛み,過敏症,およびアロディニアにつながる.
- N-メチル-D-アスパルテート (NMDA) 型グルタミン酸受容体は,脊髄におけるこれらの痛みの変化を媒介する.
研究 の 目的:
- 痛みのシグナル伝達と脊髄のニューロン変化におけるNMDA受容体活性化の役割を調査する.
- NMDA受容体媒介の痛みにおける物質Pの関与を調査する.
主な方法:
- ネズミの脊髄の脳脊髄液にNMDAを注入する.
- P受容体アンタゴニスト物質の投与.
- カプサイシンを用いた物質Pを含む繊維の除去.
主要な成果:
- NMDAの活性化により,痛み,物質Pの放出,背部の角のニューロンにおける受容体の内部化が引き起こされた.
- 背部の角のニューロンで構造的デンドリット変化が観察されました.
- 物質P受容体アンタゴニストとカプサイシンは,NMDA誘発の痛みと形態学的変化を著しく軽減しました.
結論:
- 疼痛繊維のプレシナプス性NMDA受容体は,物質Pとグルタミン酸の放出を通じて,痛覚伝達を促進します.
- プレシナプス性NMDA受容体へのターゲティングは,外傷による持続的な痛みに対する潜在的な治療戦略を提供します.
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