The NaV1.7 sodium channel: from molecule to man

被引：434
|
作者：
Dib-Hajj, Sulayman D. [1 ,2 ,3 ]
Yang, Yang [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 | 2013年 / 14卷 / 01期
关键词：
VOLTAGE-GATED SODIUM; EXTREME PAIN DISORDER; CLOSED-STATE INACTIVATION; OF-FUNCTION MUTATIONS; ROOT GANGLION NEURONS; NEUROPATHIC PAIN; SENSORY NEURONS; ELECTROPHYSIOLOGICAL PROPERTIES; SLOW-INACTIVATION; PHARMACOLOGICAL MANAGEMENT;
D O I：
10.1038/nrn3404
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
The voltage-gated sodium channel Na(V)1.7 is preferentially expressed in peripheral somatic and visceral sensory neurons, olfactory sensory neurons and sympathetic ganglion neurons. Na(V)1.7 accumulates at nerve fibre endings and amplifies small subthreshold depolarizations, poising it to act as a threshold channel that regulates excitability. Genetic and functional studies have added to the evidence that Na(V)1.7 is a major contributor to pain signalling in humans, and homology modelling based on crystal structures of ion channels suggests an atomic-level structural basis for the altered gating of mutant Na(V)1.7 that causes pain.
引用
收藏
页码：49 / 62
页数：14
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