ArticleCirculation research2012
Functional Nav1.8 channels in intracardiac neurons: the link between SCN10A and cardiac electrophysiology.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
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Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- Common and Rare Coding Genetic Variation Underlying the Electrocardiographic PR Interval.Circulation. Genomic and precision medicine · 2018Pooled it
- Common and rare variants in SCN10A modulate the risk of atrial fibrillation.Circulation. Cardiovascular genetics · 2015Trial
- Genome- and phenome-wide analyses of cardiac conduction identifies markers of arrhythmia risk.Circulation · 2013Trial
- A neurocutaneous NaScience advances · 2026Article
- From ion channel biology to clinical practice: suzetrigine as a precision analgesic.Frontiers in medicine · 2026Review
- MOG1medRxiv : the preprint server for health sciences · 2025Article
- Isoform-specific N-linked glycosylation of NaV channel α-subunits alters β-subunit binding sites.The Journal of general physiology · 2025Article
- Characterization of novel arrhythmogenic patterns arising secondary to heterogeneous expression and activation of Nav1.8.Frontiers in cardiovascular medicine · 2025Article
- ZnO nanoparticles induce acute arrhythmia and heart failure in mice by disturbing cardiac ion channels.Frontiers in cardiovascular medicine · 2025Article
- Remodeling of the Intracardiac Ganglia During the Development of Cardiovascular Autonomic Dysfunction in Type 2 Diabetes: Molecular Mechanisms and Therapeutics.International journal of molecular sciences · 2024Review
- Blocking NaBMC cardiovascular disorders · 2024Article
- Insights into the voltage-gated sodium channel, NaFrontiers in pharmacology · 2024Review
- Review
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- Patient-specific induced pluripotent stem cell properties implicate CaPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
- Cardiac sodium channel complexes and arrhythmia: structural and functional roles of the β1 and β3 subunits.The Journal of physiology · 2023Article
- Brugada Syndrome: From Molecular Mechanisms and Genetics to Risk Stratification.International journal of molecular sciences · 2023Review
- Deep learning-derived cardiovascular age shares a genetic basis with other cardiac phenotypes.Scientific reports · 2022Article
- Late Sodium Current of the Heart: Where Do We Stand and Where Are We Going?Pharmaceuticals (Basel, Switzerland) · 2022Review
- Overlap Arrhythmia Syndromes Resulting from Multiple Genetic Variations Studied in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes.International journal of molecular sciences · 2021Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleThe SCN10A gene encodes the neuronal sodium channel isoform Na(V)1.8. Several recent genome-wide association studies have linked SCN10A to PR interval and QRS duration, strongly suggesting an as-yet unknown role for Na(V)1.8 in cardiac electrophysiology.
objectiveTo demonstrate the functional presence of SCN10A/Nav1.8 in intracardiac neurons of the mouse heart. METHODS AND
resultsImmunohistochemistry on mouse tissue sections showed intense Na(V)1.8 labeling in dorsal root ganglia and intracardiac ganglia and only modest Na(V)1.8 expression within the myocardium. Immunocytochemistry further revealed substantial Na(V)1.8 staining in isolated neurons from murine intracardiac ganglia but no Na(V)1.8 expression in isolated ventricular myocytes. Patch-clamp studies demonstrated that the Na(V)1.8 blocker A-803467 (0.5-2 μmol/L) had no effect on either mean sodium current (I(Na)) density or I(Na) gating kinetics in isolated myocytes but significantly reduced I(Na) density in intracardiac neurons. Furthermore, A-803467 accelerated the slow component of current decay and shifted voltage dependence of inactivation toward more negative voltages, as expected for blockade of Na(V)1.8-based I(Na). In line with these findings, A-803467 did not affect cardiomyocyte action potential upstroke velocity but markedly reduced action potential firing frequency in intracardiac neurons, confirming a functional role for Na(V)1.8 in cardiac neural activity.
conclusionsOur findings demonstrate the functional presence of SCN10A/Na(V)1.8 in intracardiac neurons, indicating a novel role for this neuronal sodium channel in regulation of cardiac electric activity.
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