ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Kv1.1 potassium channel deficiency reveals brain-driven cardiac dysfunction as a candidate mechanism for sudden unexplained death in epilepsy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.
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128 citing papers in PubMed, 1 synthesis or guideline pooled it, 232 citations in OpenAlex.
- Systematic Review of the Genetics of Sudden Unexpected Death in Epilepsy: Potential Overlap With Sudden Cardiac Death and Arrhythmia-Related Genes.Journal of the American Heart Association · 2020Pooled it
- Small-Conductance CaNeuroscience bulletin · 2026Review
- High-frequency oscillations arise through distinct mechanisms in models of α- synucleinopathy and channelopathy-induced epilepsy.Research square · 2026Article
- Sex-specific differences in mortality and neurocardiac interactions in the Kv1.1 knockout mouse model of sudden unexpected death in epilepsy (SUDEP).The Journal of physiology · 2026Article
- Article
- Cardiac-specific Kv1.1 deficiency alters cardiomyocyte electrophysiology without modifying overall cardiac function or arrhythmia susceptibility.Experimental physiology · 2026Article
- Shaker potassium channel mediates an age-sensitive neurocardiac axis regulating sleep and cardiac function in Drosophila.Biogerontology · 2026Article
- Inflammation modifies breathing phenotype in mice with epilepsy.Journal of neuroinflammation · 2026Article
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- Early death and neuronal abnormalities inbioRxiv : the preprint server for biology · 2025Article
- Enhancing sudden unexpected death in epilepsy (SUDEP) research through development of common data elements.Epilepsia open · 2025Article
- The Crucial Interplay Between the Lungs, Brain, and Heart to Understand Epilepsy-Linked SUDEP: A Literature Review.Brain sciences · 2025Review
- Sudden Unexpected Death in Epilepsy: A Narrative Review of Mechanism, Risks, and Prevention.Journal of clinical medicine · 2025Review
- Spotlight on mechanism of sudden unexpected death in epilepsy in Dravet syndrome.Translational psychiatry · 2025Review
- SUMO Regulation of Ion Channels in Health and Disease.Physiology (Bethesda, Md.) · 2025Review
- Sudden Unexpected Death in Epilepsy: Central Respiratory Chemoreception.International journal of molecular sciences · 2025Review
- Seizures and premature death in mice with targeted Kv1.1 deficiency in corticolimbic circuits.Brain communications · 2025Article
- Transgenic mice overexpressing Pitx2 in the atria develop tachycardia-bradycardia syndrome.PloS one · 2025Article
- Metabolic aspects of genetic ion channel epilepsies.Journal of neurochemistry · 2024Review
- Epilepsy-associated Kv1.1 channel subunits regulate intrinsic cardiac pacemaking in mice.The Journal of general physiology · 2024Article
68 more citing papers are in PubMed but not listed here.
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5 authors at 1 institution in 1 country.
Funding
Abstract
Mice lacking Kv1.1 Shaker-like potassium channels encoded by the Kcna1 gene exhibit severe seizures and die prematurely. The channel is widely expressed in brain but only minimally, if at all, in mouse myocardium. To test whether Kv1.1-potassium deficiency could underlie primary neurogenic cardiac dysfunction, we performed simultaneous video EEG-ECG recordings and found that Kcna1-null mice display potentially malignant interictal cardiac abnormalities, including a fivefold increase in atrioventricular (AV) conduction blocks, as well as bradycardia and premature ventricular contractions. During seizures the occurrence of AV conduction blocks increased, predisposing Kv1.1-deficient mice to sudden unexplained death in epilepsy (SUDEP), which we recorded fortuitously in one animal. To determine whether the interictal AV conduction blocks were of cardiac or neural origin, we examined their response to selective pharmacological blockade of the autonomic nervous system. Simultaneous administration of atropine and propranolol to block parasympathetic and sympathetic branches, respectively, eliminated conduction blocks. When administered separately, only atropine ameliorated AV conduction blocks, indicating that excessive parasympathetic tone contributes to the neurocardiac defect. We found no changes in Kv1.1-deficient cardiac structure, but extensive Kv1.1 expression in juxtaparanodes of the wild-type vagus nerve, the primary source of parasympathetic input to the heart, suggesting a novel site of action leading to Kv1.1-associated cardiac bradyarrhythmias. Together, our data suggest that Kv1.1 deficiency leads to impaired neural control of cardiac rhythmicity due in part to aberrant parasympathetic neurotransmission, making Kcna1 a strong candidate gene for human SUDEP.
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