Article
Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Nav1.7 mutation that massively hyperpolarizes activation.
Scientific reports - 29 Jan 2018
Huang Jianying, Mis Malgorzata A, Tanaka Brian, Adi Talia, Estacion Mark, Liu Shujun, Walker Suellen, Dib-Hajj Sulayman D, Waxman Stephen G
Abstract excerpt
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 pain, together with absence of pain following fractures, and corneal anesthesia. How a Nav1.7 mutation that produces...
Topics
- Animals
- Cell Line
- Female
- Ganglia, Spinal
- HEK293 Cells
- Humans
- Male
- Membrane Potentials
- Mutation
- NAV1.7 Voltage-Gated Sodium Channel
- Neurons