Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8.
Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8.
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DOI：
10.1186/1744-8069-1-24
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发表时间：
2005-08-22
期刊：
影响因子：
3.3
通讯作者：
Wood JN
中科院分区：
文献类型：
--
作者：
Nassar MA;Levato A;Stirling LC;Wood JN
两个电压门控钠通道α-亚基Nav1.7和Nav1.8在伤害感受器末端高水平表达，并与炎症性疼痛的发生有关。受损感觉神经元电压门控钠通道的错误表达也与神经性疼痛的发生有关，但Nav1.7和Nav1.8的作用尚不确定。本研究表明，删除Nav1.7对神经性疼痛的发展没有影响。Nav1.7和Nav1.8的双敲除也会产生正常水平的神经性疼痛，尽管缺乏炎症性疼痛症状和改变的机械和热急性疼痛阈值。这些研究表明，与Nav1.7在决定炎症性疼痛阈值中的高度重要作用相反，神经性疼痛的发生不需要Nav1.7或Nav1.8单独或联合存在。
Two voltage gated sodium channel α-subunits, Nav1.7 and Nav1.8, are expressed at high levels in nociceptor terminals and have been implicated in the development of inflammatory pain. Mis-expression of voltage-gated sodium channels by damaged sensory neurons has also been implicated in the development of neuropathic pain, but the role of Nav1.7 and Nav1.8 is uncertain. Here we show that deleting Nav1.7 has no effect on the development of neuropathic pain. Double knockouts of both Nav1.7 and Nav1.8 also develop normal levels of neuropathic pain, despite a lack of inflammatory pain symptoms and altered mechanical and thermal acute pain thresholds. These studies demonstrate that, in contrast to the highly significant role for Nav1.7 in determining inflammatory pain thresholds, the development of neuropathic pain does not require the presence of either Nav1.7 or Nav1.8 alone or in combination.
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影响因子：
5.5
作者：
Brock, JA;McLachlan, EM;Belmonte, C
通讯作者：
Belmonte, C
影响因子：
1.7
作者：
Kerr, BJ;Souslova, V;Wood, JN
通讯作者：
Wood, JN
DOI：
10.1016/s0169-328x(96)00241-0
发表时间：
1997-04-01
期刊：
MOLECULAR BRAIN RESEARCH
影响因子：
--
作者：
Felts, PA;Yokoyama, S;Waxman, SG
通讯作者：
Waxman, SG
影响因子：
7.4
作者：
Flake, NM;Lancaster, E;Gold, MS
通讯作者：
Gold, MS
影响因子：
8.8
作者：
CHABAL, C;JACOBSON, L;LITTLE, J
通讯作者：
LITTLE, J