A role for the TTX-resistant sodium channel Nav 1.8 in NGF-induced hyperalgesia, but not neuropathic pain
A role for the TTX-resistant sodium channel Nav 1.8 in NGF-induced hyperalgesia, but not neuropathic pain
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DOI：
10.1097/00001756-200110080-00019
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发表时间：
2001-10-08
期刊：
影响因子：
1.7
通讯作者：
Wood, JN
中科院分区：
文献类型：
--
作者：
Kerr, BJ;Souslova, V;Wood, JN
河豚毒素抗性电压门控钠通道NAV1.8仅在伤害性感觉神经元表达。这一通道被认为对损伤后初级感觉神经元的敏化有重要贡献。我们研究了NAV 1.8基因零突变(NAV 1.8-/-)小鼠在外周炎症模型和神经病理性疼痛模型中的伤害性行为。本研究结果表明，NAV1.8是NGF诱导的热痛觉过敏的必需介质，但对PGE(2)诱导的超敏反应不是必需的。在NAV1.8-/-小鼠中，神经病理性疼痛行为没有变化，这表明该通道不参与周围神经损伤后感觉阈值的改变。《神经报告》12：3077-3080(C)2001，Lippincott Williams&Wilkins.
The tetrodotoxin-resistant voltage-gated sodium channel Nav 1.8 is expressed only in nociceptive sensory neurons. This channel has been proposed to contribute significantly to the sensitization of primary sensory neurons after injury. We have studied the nociceptive behaviours of mice carrying a null mutation in the Nav 1.8 gene (Nav 1.8 -/-) in models of peripheral inflammation as well as a model of neuropathic pain. The results from the present studies reveal that Nav 1.8 is a necessary mediator of NGF-induced thermal hyperalgesia but is not essential for PGE(2)-evoked hypersensitivity. Neuropathic pain behaviours were unchanged in Nav 1.8 -/- mice indicating that this channel is not involved in the alteration of sensory thresholds following peripheral nerve injury. NeuroReport 12:3077-3080 (C) 2001 Lippincott Williams & Wilkins.