Kerr B J, Souslova V, McMahon S B, Wood J N
Centre for Neuroscience Research, Guy's, King's and St Thomas' School of Biomedical Sciences, Kings College, London SE1 1UL, UK.
Neuroreport. 2001 Oct 8;12(14):3077-80. doi: 10.1097/00001756-200110080-00019.
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 PGE2-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.
抗河豚毒素的电压门控钠通道Nav 1.8仅在伤害性感觉神经元中表达。有人提出该通道在损伤后对初级感觉神经元的敏化有显著作用。我们在周围炎症模型以及神经性疼痛模型中研究了Nav 1.8基因发生无效突变的小鼠（Nav 1.8 -/-）的伤害性行为。本研究结果表明，Nav 1.8是NGF诱导的热痛觉过敏的必要介质，但对PGE2诱发的超敏反应并非必不可少。Nav 1.8 -/-小鼠的神经性疼痛行为未发生改变，这表明该通道不参与周围神经损伤后感觉阈值的改变。
