ArticleJournal of molecular neuroscience : MN2005
A TASK3 channel (KCNK9) mutation in a genetic model of absence epilepsy.
Article in Journal of molecular neuroscience : MN, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 35 citations in OpenAlex.
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- Etiological Diagnosis and Disease Course of Birk-Barel Syndrome in an Adult Woman with aInternational medical case reports journal · 2026Article
- The Effects of Overexpressing K2p Channels in Various Tissues on Physiology and Behaviors.Insects · 2025Article
- Genetic Animal Models of Idiopathic Generalized Epilepsies: What Can We Learn from Them?Biomedicines · 2025Review
- Scavenger Receptor Class B Type I Modulates Epileptic Seizures and Receptor α2δ-1 Expression.Neurochemical research · 2024Article
- Hyperpolarization Induced by Lipopolysaccharides but Not by Chloroform Is Inhibited by Doxapram, an Inhibitor of Two-P-Domain KInternational journal of molecular sciences · 2022Article
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- Contribution of Neuronal and Glial Two-Pore-Domain Potassium Channels in Health and Neurological Disorders.Neural plasticity · 2021Review
- Regulatory Architecture of the Neuronal Cacng2/Tarpγ2 Gene Promoter: Multiple Repressive Domains, a Polymorphic Regulatory Short Tandem Repeat, and Bidirectional Organization with Co-regulated lncRNAs.Journal of molecular neuroscience : MN · 2019Article
- Genetic and epigenetic mechanisms of epilepsy: a review.Neuropsychiatric disease and treatment · 2017Review
- Potassium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016Review
- Thalamocortical neurons display suppressed burst-firing due to an enhanced Ih current in a genetic model of absence epilepsy.Pflugers Archiv : European journal of physiology · 2015Article
- Rhythm and blues: animal models of epilepsy and depression comorbidity.Biochemical pharmacology · 2013Review
- Mutation Screening of the γ-Aminobutyric Acid Type-A Receptor Subunit γ2 Gene in Korean Patients with Childhood Absence Epilepsy.Journal of clinical neurology (Seoul, Korea) · 2012Article
- Frequent missense and insertion/deletion polymorphisms in the ovine Shadoo gene parallel species-specific variation in PrP.PloS one · 2009Article
- A Cav3.2 T-type calcium channel point mutation has splice-variant-specific effects on function and segregates with seizure expression in a polygenic rat model of absence epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- TASK3 and its role in neuro and systemic oncogenesis.Journal of neuro-oncology · 2008Article
- Molecular targets for antiepileptic drug development.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2007Review
- Functional stabilization of weakened thalamic pacemaker channel regulation in rat absence epilepsy.The Journal of physiology · 2006Article
- Identification of two further splice variants of GABABR1 characterizes the conserved micro-exon 4 as a hot spot for regulated splicing in the rat brain.Journal of molecular neuroscience : MN · 2005Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Childhood absence epilepsy is an idiopathic, generalized, nonconvulsive epilepsy with a multifactorial genetic etiology. The KCNK9 gene coding for the TASK3 (Twik-like acid-sensitive K</U)+) channel is present on chromosome 8 at position 8q24, a locus that has shown positive linkage to the human absence epilepsy phenotype. Sequencing of the KCNK9 gene in the genetic absence epilepsy rats from Strasbourg (GAERS), a well established genetic model of this disease, reveals an additional alanine residue in a polyalanine tract within the C-terminal intracellular domain. This additional alanine is absent in the inbred nonepileptic control (NEC) strain, Wistar, and Wistar albino Glaxo strain bred in Rijswijk, another inbred rat model of absence epilepsy. Expression of the mutant channel in CHO cells produces a K+ current that is blocked by acidic pH and millimolar concentrations of barium or ruthenium red and is not different from the wild-type channel. In brain slices, thalamic neurons display a prominent pH-sensitive tonic K+ current, but no difference was observed between GAERS and NEC or Wistar rats. Ruthenium red had no effect in cortical, reticular thalamic, or sensory thalamic neurons in either GAERS or NEC, indicating that the TASK3 homodimer is not present in these structures. Twik-like acid-sensitive K+(TASK3) channels, therefore, are probably associated with TASK1 to form ruthenium red-insensitive heterodimers in these neurons. Finally, no difference was found between GAERS and NEC rats in the modulation of the leak K+ current following activation of muscarinic receptors. These studies describe the first mutation found in a genetic model of absence epilepsy. Although our experiments showed no difference in the leak K+ current between GAERS and NEC rats, further work is needed to ascertain whether this mutation contributes to the generation of absence seizures, possibly by mechanisms related to the expansion of the polyalanine run.
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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.