NaV 1.9: a sodium channel linked to human pain

被引：151

作者：

Dib-Hajj, Sulayman D. ^{[1
,2
,3
]}

Black, Joel A. ^{[1
,2
,3
]}

Waxman, Stephen G. ^{[1
,2
,3
]}

机构：

[1] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06510 USA

[2] Yale Univ, Sch Med, Ctr Neurosci & Regenerat Res, New Haven, CT 06510 USA

[3] Vet Affairs Connecticut Healthcare Syst, Rehabil Res Ctr, West Haven, CT 06516 USA

来源：

NATURE REVIEWS NEUROSCIENCE | 2015年 / 16卷 / 09期

关键词：

ROOT GANGLION NEURONS; OF-FUNCTION MUTATIONS; NA(V)1.8 MUTATION; SENSORY NEURONS; VOLTAGE SENSOR; RESISTANT; NAV1.9; MOUSE; NOCICEPTORS; EXPRESSION;

D O I：

10.1038/nrn3977

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

The voltage-gated sodium channel Na(V)1.9 is preferentially expressed in nociceptors and has been shown in rodent models to have a major role in inflammatory and neuropathic pain. These studies suggest that by selectively targeting Na(V)1.9, it might be possible to ameliorate pain without inducing adverse CNS side effects such as sedation, confusion and addictive potential. Three recent studies in humans - two genetic and functional studies in rare genetic disorders, and a third study showing a role for Na(V)1.9 in painful peripheral neuropathy have demonstrated that Na(V)1.9 plays an important part both in regulating sensory neuron excitability and in pain signalling. With this human validation, attention is turning to this channel as a potential therapeutic target for pain.

引用

收藏

页码：511 / 519

页数：9

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