感覚神経のナトリウムチャンネルNav1.8は,低温での痛みに不可欠です
Katharina Zimmermann1, Andreas Leffler, Alexandru Babes
1Department of Physiology and Pathophysiology, Faculty of Medicine, Friedrich-Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany. zimmermann@physiologie1.uni-erlangen.de
Nature
|June 15, 2007
まとめ
ボルテージゲートナトリウムチャネルNa(v) 1.8は,風邪の痛みを検知するために不可欠です. この経路は低温でも機能し,痛覚受容体が痛みの信号を伝達することを可能にします.
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.
- 生理学 生理学とは
背景:
- 寒さへの曝露は,感覚と運動機能を損なう.
- 痛みの知覚,特に寒さによる痛みは持続し,重症になる可能性があります.
- ノイシセプターは,低温で機能し,保護行動を確保しなければなりません.
研究 の 目的:
- 低温でノシセプター機能を可能にする分子メカニズムを調査する.
- 冷たい痛みの知覚に責任を負う特定の電圧ゲートされたナトリウムチャネルを特定するために.
主な方法:
- 異なる温度下での電圧ゲートナトリウムチャネル (VGSC) の性質を調べました.
- テトロドトキシンに敏感なVGSCとNa ((v) 1.8.8.) の不活性化特性を調査しました.
- 寒さや機械的刺激に対する反応を評価するために,Na(v) 1.8-null変異マウスを利用した.
主要な成果:
- テトロドトキシンに敏感なVGSCは,低温で遅い無活性化が強化されています.
- Na(v) 1.8は,冷却に耐える不活性化特性を持ち,機能を維持しています.
- 低温では,Na (v) 1.8の活性化値が低下し,膜抵抗が増加し,信号伝送が強化される.
- Na(v) 1.8-nullのマウスは,低温で有害な寒さや機械的刺激に対する反応を著しく低下させた.
結論:
- Na(v) 1.8は,冷たい環境下での持続的な神経受容体の興奮性と機能に不可欠です.
- Na(v) 1.8は,冷たい痛みの信号を伝達するための主要な電気インパルス発生器として機能します.
- Na(v) 1.8は,冷たい痛みの知覚に重要な役割を果たしています.
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