ArticleThe Journal of clinical investigation2010
Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 143 citations in OpenAlex.
- Inherited pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation.The Journal of biological chemistry · 2014Trial
- Sea-anemone toxin ATX-II elicits A-fiber-dependent pain and enhances resurgent and persistent sodium currents in large sensory neurons.Molecular pain · 2012Trial
- The Bright Side of the Spectrum: Self-Limited Infantile Epilepsy-Related SCN8A Gof Variant.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2026Article
- Contusive spinal cord injury causes Nav1.8 dysfunction to upregulate small sensory neuron excitability.The Journal of physiology · 2025Article
- Effects of open-channel blocking peptides in NaBiophysical journal · 2025Article
- A Case Report of Encephalopathy With Myoclonus: A Rare Neurologic Side Effect of Ranolazine.Cureus · 2025Article
- Parvalbumin interneuron impairment causes synaptic transmission deficits and seizures in SCN8A developmental and epileptic encephalopathy.JCI insight · 2024Article
- A Reinterpretation of the Relationship between Persistent and Resurgent Sodium Currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Resurgent current in context: Insights from the structure and function of Na and K channels.Biophysical journal · 2024Review
- A Reinterpretation of the Relationship Between Persistent and Resurgent Sodium Currents.bioRxiv : the preprint server for biology · 2024Article
- Special electromyographic features in a child with paramyotonia congenita: A case report and review of literature.World journal of clinical cases · 2024Article
- Molecular determinants of resurgent sodium currents mediated by Navβ4 peptide and A-type FHFs.Frontiers in molecular neuroscience · 2024Article
- Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents.The Journal of general physiology · 2023Article
- Structure of human NaNature communications · 2023Article
- Chemical and Biological Tools for the Study of Voltage-Gated Sodium Channels in Electrogenesis and Nociception.Chembiochem : a European journal of chemical biology · 2022Review
- Article
- A-type FHFs mediate resurgent currents through TTX-resistant voltage-gated sodium channels.eLife · 2022Article
- Article
- Local hyperexcitability of C-nociceptors may predict responsiveness to topical lidocaine in neuropathic pain.PloS one · 2022Article
- Changes in Resurgent Sodium Current Contribute to the Hyperexcitability of Muscles in Patients with Paramyotonia Congenita.Biomedicines · 2021Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inherited mutations in voltage-gated sodium channels (VGSCs; or Nav) cause many disorders of excitability, including epilepsy, chronic pain, myotonia, and cardiac arrhythmias. Understanding the functional consequences of the disease-causing mutations is likely to provide invaluable insight into the roles that VGSCs play in normal and abnormal excitability. Here, we sought to test the hypothesis that disease-causing mutations lead to increased resurgent currents, unusual sodium currents that have not previously been implicated in disorders of excitability. We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Computer simulations indicated that resurgent currents associated with the Nav1.7 mutation could induce high-frequency action potential firing in nociceptive neurons and that resurgent currents associated with the Nav1.5 mutation could broaden the action potential in cardiac myocytes. These effects are consistent with the pathophysiology associated with the respective channelopathies. Our results indicate that resurgent currents are associated with multiple channelopathies and are likely to be important contributors to neuronal and muscle disorders of excitability.
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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.