Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Nav1.7 mutation that massively hyperpolarizes activation

Abstract Sodium channel Nav1.7 plays a central role in pain-signaling: gain-of-function Nav1.7 mutations usually cause severe pain and loss-of-function mutations produce insensitivity to pain. The Nav1.7 I234T gain-of-function mutation, however, is linked to a dual clinical presentation of episodic...

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Autores principales: Jianying Huang, Malgorzata A. Mis, Brian Tanaka, Talia Adi, Mark Estacion, Shujun Liu, Suellen Walker, Sulayman D. Dib-Hajj, Stephen G. Waxman
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/8eca63acbcfb47469d32f11de63ac492
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