ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012
A null mutation of the neuronal sodium channel NaV1.6 disrupts action potential propagation and excitation-contraction coupling in the mouse heart.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Sodium Channel Isoform Diversity Underlies Chamber-Specific Cardiac Excitability.Circulation research · 2026Article
- FGF14 Peptide Derivative Differentially Regulates Nav1.2 and NaLife (Basel, Switzerland) · 2025Article
- Social Determinants of Health in Cardio-Oncology: Multi-Level Strategies to Overcome Disparities in Care:JACC. CardioOncology · 2024Review
- Gene mutations in comorbidity of epilepsy and arrhythmia.Journal of neurology · 2023Review
- Single-neuron models linking electrophysiology, morphology, and transcriptomics across cortical cell types.Cell reports · 2022Article
- Review
- Mexiletine-like cellular electrophysiological effects of GS967 in canine ventricular myocardium.Scientific reports · 2021Article
- In vitro and in vivo cardiac toxicity of flavored electronic nicotine delivery systems.American journal of physiology. Heart and circulatory physiology · 2021Article
- Article
- Epilepsy-Related Voltage-Gated Sodium Channelopathies: A Review.Frontiers in pharmacology · 2020Review
- SCN8A encephalopathy: Mechanisms and models.Epilepsia · 2019Review
- A privileged role for neuronal NaThe Journal of general physiology · 2018Article
- Tetrodotoxin-sensitive NaThe Journal of general physiology · 2018Article
- Cardiac T-Tubule Microanatomy and Function.Physiological reviews · 2017Review
- Cardiac arrhythmia in a mouse model of sodium channelProceedings of the National Academy of Sciences of the United States of America · 2016Article
- Genetic biomarkers for the risk of seizures in long QT syndrome.Neurology · 2016Article
- SCN8A encephalopathy: Research progress and prospects.Epilepsia · 2016Article
- Extracellular Matrix-Mediated Maturation of Human Pluripotent Stem Cell-Derived Cardiac Monolayer Structure and Electrophysiological Function.Circulation. Arrhythmia and electrophysiology · 2016Article
- Pathogenic mechanism of recurrent mutations of SCN8A in epileptic encephalopathy.Annals of clinical and translational neurology · 2016Article
- EXPRESS: Voltage-dependent sodium (NaV) channels in group IV sensory afferents.Molecular pain · 2016Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Evidence supports the expression of brain-type sodium channels in the heart. Their functional role, however, remains controversial. We used global Na(V)1.6-null mice to test the hypothesis that Na(V)1.6 contributes to the maintenance of propagation in the myocardium and to excitation-contraction (EC) coupling. We demonstrated expression of transcripts encoding full-length Na(V)1.6 in isolated ventricular myocytes and confirmed the striated pattern of Na(V)1.6 fluorescence in myocytes. On the ECG, the PR and QRS intervals were prolonged in the null mice, and the Ca(2+) transients were longer in the null cells. Under patch clamping, at holding potential (HP) = -120 mV, the peak I(Na) was similar in both phenotypes. However, at HP = -70 mV, the peak I(Na) was smaller in the nulls. In optical mapping, at 4 mM [K(+)](o), 17 null hearts showed slight (7%) reduction of ventricular conduction velocity (CV) compared to 16 wild-type hearts. At 12 mM [K(+)](o), CV was 25% slower in a subset of 9 null vs. 9 wild-type hearts. These results highlight the importance of neuronal sodium channels in the heart, whereby Na(V)1.6 participates in EC coupling, and represents an intrinsic depolarizing reserve that contributes to excitation.
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