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Article

Dynamic-clamp analysis of wild-type human Nav1.7 and erythromelalgia mutant channel L858H.

Journal of neurophysiology - 1 Apr 2014

Vasylyev Dmytro V, Han Chongyang, Zhao Peng, Dib-Hajj Sulayman, Waxman Stephen G

Abstract excerpt

The link between sodium channel Nav1.7 and pain has been strengthened by identification of gain-of-function mutations in patients with inherited erythromelalgia (IEM), a genetic model of neuropathic pain in humans. A firm mechanistic link to nociceptor dysfunction has been precluded because assessments of the effect of the mutations on nociceptor function have thus far depended on electrophysiological recordings...

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Source

Identifiers

PMID: 24401712
DOI: 10.1152/jn.00763.2013

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Dynamic-clamp analysis of wild-type human Nav1.7 and erythromelalgia mutant channel L858H.PMID 24401712Read ↗

Nonlinear effects of hyperpolarizing shifts in activation of mutant Nav1.7 channels on resting membrane potential.Semantic proximity Read ↗

Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons.Semantic proximity Read ↗

Stem cell-derived sensory neurons modelling inherited erythromelalgia: normalization of excitability.Semantic proximity Read ↗

Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons.Semantic proximity Read ↗

Nav1.7-A1632G Mutation from a Family with Inherited Erythromelalgia: Enhanced Firing of Dorsal Root Ganglia Neurons Evoked by Thermal Stimuli.Semantic proximity Read ↗

Novel mutations mapping to the fourth sodium channel domain of Nav1.7 result in variable clinical manifestations of primary erythromelalgia.Semantic proximity Read ↗

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

NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders.Semantic proximity Read ↗

Pain disorders and erythromelalgia caused by voltage-gated sodium channel mutations.Semantic proximity Read ↗

A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons.Semantic proximity Read ↗

Erythromelalgia mutation L823R shifts activation and inactivation of threshold sodium channel Nav1.7 to hyperpolarized potentials.Semantic proximity Read ↗

Depolarized inactivation overcomes impaired activation to produce DRG neuron hyperexcitability in a Nav1.7 mutation in a patient with distal limb pain.Semantic proximity Read ↗

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