ArticleProceedings of the National Academy of Sciences of the United States of America2006
A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 1 of them a synthesis that pooled it.
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Who cites it
170 citing papers in PubMed, 1 synthesis or guideline pooled it, 403 citations in OpenAlex.
- Comparative Efficacy and Tolerability of Treatments for Erythromelalgia: A Systematic Review.Medicina (Kaunas, Lithuania) · 2025Pooled it
- Inherited pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation.The Journal of biological chemistry · 2014Trial
- Ultraviolet-B sensitizes silent nociceptors and desensitizes C-touch fibers to slow depolarizing electrical stimuli in pigs.Pain reports · 2026Article
- Functional role of Nav1.8 channels in action potentials of mouse CGRP-lineage dorsal root ganglion neurons.The Journal of physiology · 2026Article
- Nav1.8 Variant I206M as a Latent Susceptibility Factor in Postaxotomy Ocular Pain.Neurology. Genetics · 2026Article
- Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- Co-Occurrence ofCase reports in medicine · 2026Article
- Article
- Targeting sodium channels - challenges for acute pain and the leap to chronic pain.Nature reviews. Neurology · 2025Review
- Nav1.8: Intrinsic limits on the functional effect of abrogation in DRG neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- SCN9A should not be considered an epilepsy gene; Refuting a gene-disease association.Epilepsia · 2025Article
- Differential state-dependent Nav1.8 inhibition by suzetrigine, LTGO-33, and A-887826.The Journal of general physiology · 2025Article
- Inhibiting Nav1.8 for pain: Lessons from patients and from neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nav1.8 and Chronic Pain: From Laboratory Animals to Clinical Patients.Biomolecules · 2025Review
- Preclinical Animal Models to Investigate the Role of NaLife (Basel, Switzerland) · 2025Review
- Nociceptor sodium channels shape subthreshold phase, upstroke, and shoulder of action potentials.The Journal of general physiology · 2025Article
- ML-based Models as a Strategy to Discover Novel Antiepileptic Drugs Targeting Sodium Receptor Channel.Current topics in medicinal chemistry · 2025Article
- Interplay of Nav1.8 and Nav1.7 channels drives neuronal hyperexcitability in neuropathic pain.The Journal of general physiology · 2024Article
- Heterozygous expression of aeLife · 2024Article
- Heterozygous expression of abioRxiv : the preprint server for biology · 2024Article
110 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Disease-producing mutations of ion channels are usually characterized as producing hyperexcitability or hypoexcitability. We show here that a single mutation can produce hyperexcitability in one neuronal cell type and hypoexcitability in another neuronal cell type. We studied the functional effects of a mutation of sodium channel Nav1.7 associated with a neuropathic pain syndrome, erythermalgia, within sensory and sympathetic ganglion neurons, two cell types where Nav1.7 is normally expressed. Although this mutation depolarizes resting membrane potential in both types of neurons, it renders sensory neurons hyperexcitable and sympathetic neurons hypoexcitable. The selective presence, in sensory but not sympathetic neurons, of the Nav1.8 channel, which remains available for activation at depolarized membrane potentials, is a major determinant of these opposing effects. These results provide a molecular basis for the sympathetic dysfunction that has been observed in erythermalgia. Moreover, these findings show that a single ion channel mutation can produce opposing phenotypes (hyperexcitability or hypoexcitability) in the different cell types in which the channel is expressed.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.