ArticleMolecular pain2007
Temperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7.
Article in Molecular pain, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Comparative Efficacy and Tolerability of Treatments for Erythromelalgia: A Systematic Review.Medicina (Kaunas, Lithuania) · 2025Pooled it
- The Excelsatoxin A-Receptor TMEM233 Modulates Nav1.8.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Reverse-engineered models reveal differential membrane properties of autonomic and cutaneous unmyelinated fibers.PLoS computational biology · 2024Article
- Neanderthal introgression in SCN9A impacts mechanical pain sensitivity.Communications biology · 2023Article
- Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents.The Journal of general physiology · 2023Article
- Macromolecular rate theory explains the temperature dependence of membrane conductance kinetics.Biophysical journal · 2023Article
- Investigating genotype-phenotype relationship of extreme neuropathic pain disorders in a UK national cohort.Brain communications · 2023Article
- Anomalous enhancement of resurgent NaScientific reports · 2019Article
- Atypical changes in DRG neuron excitability and complex pain phenotype associated with a NaScientific reports · 2018Article
- Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability.The Journal of clinical investigation · 2017Article
- Modelling Human Colonic Smooth Muscle Cell Electrophysiology.Cellular and molecular bioengineering · 2017Article
- Network topology of NaV1.7 mutations in sodium channel-related painful disorders.BMC systems biology · 2017Article
- Modeling an Excitable Biosynthetic Tissue with Inherent Variability for Paired Computational-Experimental Studies.PLoS computational biology · 2017Article
- Cold-aggravated pain in humans caused by a hyperactive NaV1.9 channel mutant.Nature communications · 2015Article
- Mexiletine as a treatment for primary erythromelalgia: normalization of biophysical properties of mutant L858F NaV 1.7 sodium channels.British journal of pharmacology · 2014Article
- Febrile temperatures unmask biophysical defects in Nav1.1 epilepsy mutations supportive of seizure initiation.The Journal of general physiology · 2013Article
- A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockers.PloS one · 2013Article
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- Compound heterozygosity in sodium channel Nav1.7 in a family with hereditary erythermalgia.Molecular pain · 2008Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe disabling chronic pain syndrome erythromelalgia (also termed erythermalgia) is characterized by attacks of burning pain in the extremities induced by warmth. Pharmacological treatment is often ineffective, but the pain can be alleviated by cooling of the limbs. Inherited erythromelalgia has recently been linked to mutations in the gene SCN9A, which encodes the voltage-gated sodium channel Nav1.7. Nav1.7 is preferentially expressed in most nociceptive DRG neurons and in sympathetic ganglion neurons. It has recently been shown that several disease-causing erythromelalgia mutations alter channel-gating behavior in a manner that increases DRG neuron excitability.
resultsHere we tested the effects of temperature on gating properties of wild type Nav1.7 and mutant L858F channels. Whole-cell voltage-clamp measurements on wild type or L858F channels expressed in HEK293 cells revealed that cooling decreases current density, slows deactivation and increases ramp currents for both mutant and wild type channels. However, cooling differentially shifts the midpoint of steady-state activation in a depolarizing direction for L858F but not for wild type channels.
conclusionThe cooling-dependent shift of the activation midpoint of L858F to more positive potentials brings the threshold of activation of the mutant channels closer to that of wild type Nav1.7 at lower temperatures, and is likely to contribute to the alleviation of painful symptoms upon cooling in affected limbs in patients with this erythromelalgia mutation.
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