ArticleEpilepsia2018
Pharmacogenetics of KCNQ channel activation in 2 potassium channelopathy mouse models of epilepsy.
Article in Epilepsia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- 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
- Cardiac-specific Kv1.1 deficiency alters cardiomyocyte electrophysiology without modifying overall cardiac function or arrhythmia susceptibility.Experimental physiology · 2026Article
- The Crucial Interplay Between the Lungs, Brain, and Heart to Understand Epilepsy-Linked SUDEP: A Literature Review.Brain sciences · 2025Review
- Evaluation of Small-Molecule Candidates as Modulators of M-Type KInternational journal of molecular sciences · 2025Review
- Challenges and future directions of SUDEP models.Lab animal · 2024Review
- Gene mutations in comorbidity of epilepsy and arrhythmia.Journal of neurology · 2023Review
- Developmental and epileptic encephalopathies: from genetic heterogeneity to phenotypic continuum.Physiological reviews · 2023Review
- Evidence for Dual Activation ofInternational journal of molecular sciences · 2022Article
- The Effectiveness in Activating M-Type KInternational journal of molecular sciences · 2021Article
- Effective Activation by Kynurenic Acid and Its Aminoalkylated Derivatives on M-Type KInternational journal of molecular sciences · 2021Article
- Neuron-specific Kv1.1 deficiency is sufficient to cause epilepsy, premature death, and cardiorespiratory dysregulation.Neurobiology of disease · 2020Article
- Kv1.1 channel subunits in the control of neurocardiac function.Channels (Austin, Tex.) · 2019Review
- Long noncoding RNA GAS5 silencing inhibits the expression of KCNQ3 by sponging miR-135a-5p to prevent the progression of epilepsy.The Kaohsiung journal of medical sciences · 2019Article
- Altered A-type potassium channel function in the nucleus tractus solitarii in acquired temporal lobe epilepsy.Journal of neurophysiology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectivesAntiseizure drugs are the leading therapeutic choice for treatment of epilepsy, but their efficacy is limited by pharmacoresistance and the occurrence of unwanted side effects. Here, we examined the therapeutic efficacy of KCNQ channel activation by retigabine in preventing seizures and neurocardiac dysfunction in 2 potassium channelopathy mouse models of epilepsy with differing severity that have been associated with increased risk of sudden unexpected death in epilepsy (SUDEP): the Kcna1
methodsA combination of behavioral, seizure threshold, electrophysiologic, and gene expression analyses was used to determine the effects of KCNQ activation in mice.
resultsBehaviorally, Kcna1 SIGNIFICANCE: This study shows that treatment strategies in channelopathy may have unexpected outcomes and that effective rebalancing of channel defects requires improved understanding of channel interactions at the circuit and tissue levels. The efficacy of KCNQ channel activation and manifestation of adverse effects were greatly affected by genetic background, potentially limiting KCNQ modulation as a way to prevent neurocardiac dysfunction in epilepsy and thereby SUDEP risk. Our data also uncover a potential role for KCNQ2-5 channels in autonomic control of chronotropy.
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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.