NaV1.7: A central role in pain

被引:3
|
作者
Waxman, Stephen G. [1 ,2 ,3 ]
Dib-Hajj, Sulayman D. [1 ,2 ,3 ]
机构
[1] Yale Univ, Dept Neurol, New Haven, CT 06520 USA
[2] Yale Univ, Ctr Neurosci & Regenerat Res, New Haven, CT 06520 USA
[3] VA Connecticut Healthcare Syst, Ctr Rehabil Res, West Haven, CT 06516 USA
关键词
MUTATION;
D O I
10.1016/j.neuron.2023.08.011
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Loss of function of sodium channel Na(V)1.7 produces pain insensitivity. In this issue, Deng et al.(1) show that analgesia after Na(V)1.7 removal or pharmacological blockade is not driven by enkephalin overexpression. These results underscore the essential role, independent of endogenous opioids, of Na(V)1.7 for nociceptor firing and pain.
引用
收藏
页码:2615 / 2617
页数:3
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