ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Role of the alpha1G T-type calcium channel in spontaneous absence seizures in mutant mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 134 citations in OpenAlex.
- Parvalbumin interneuron activation rescues both seizures and impaired social novelty in digenic absence epilepsy mice.Science advances · 2026Article
- Article
- Genetic Animal Models of Idiopathic Generalized Epilepsies: What Can We Learn from Them?Biomedicines · 2025Review
- Voltage-gated calcium channels in genetic epilepsies.Journal of neurochemistry · 2024Review
- Molecular Mechanisms Underlying the Generation of Absence Seizures: Identification of Potential Targets for Therapeutic Intervention.International journal of molecular sciences · 2024Review
- The complex molecular epileptogenesis landscape of glioblastoma.Cell reports. Medicine · 2024Article
- Thalamocortical circuits in generalized epilepsy: Pathophysiologic mechanisms and therapeutic targets.Neurobiology of disease · 2023Review
- Altered brain state during episodic dystonia in tottering mice decouples primary motor cortex from limb kinematics.Dystonia (Lausanne, Switzerland) · 2023Article
- Controlling absence seizures from the cerebellar nuclei via activation of the GCellular and molecular life sciences : CMLS · 2022Article
- Epilepsy and episodic ataxia type 2: family study and review of the literature.Journal of neurology · 2021Review
- Different roles of T-type calcium channel isoforms in hypnosis induced by an endogenous neurosteroid epipregnanolone.Neuropharmacology · 2021Article
- The Transcription Factor Shox2 Shapes Neuron Firing Properties and Suppresses Seizures by Regulation of Key Ion Channels in Thalamocortical Neurons.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- Global genetic deletion of CaScientific reports · 2020Article
- Novel MissenseInternational journal of molecular sciences · 2020Article
- Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms.Brain : a journal of neurology · 2020Article
- Alterations in Oscillatory Behavior of Central Medial Thalamic Neurons Demonstrate a Key Role of CaV3.1 Isoform of T-Channels During Isoflurane-Induced Anesthesia.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Inhibition of human N- and T-type calcium channels by an ortho-phenoxyanilide derivative, MONIRO-1.British journal of pharmacology · 2018Article
- In vitro and in vivo phosphorylation of the CaChannels (Austin, Tex.) · 2018Review
- Ion Channels in Genetic Epilepsy: From Genes and Mechanisms to Disease-Targeted Therapies.Pharmacological reviews · 2018Review
- Models and detection of spontaneous recurrent seizures in laboratory rodents.Zoological research · 2017Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alterations in thalamic T-type Ca2+ channels are thought to contribute to the pathogenesis of absence seizures. Here, we found that mice with a null mutation for the pore-forming alpha1A subunits of P/Q-type channels (alpha1A-/- mice) were prone to absence seizures characterized by typical spike-and-wave discharges (SWDs) and behavioral arrests. Isolated thalamocortical relay (TC) neurons from these mice showed increased T-type Ca2+ currents in vitro. To examine the role of increased T-currents in alpha1A-/- TC neurons, we cross-bred alpha1A-/- mice with mice harboring a null mutation for the gene encoding alpha1G, a major isotype of T-type Ca2+ channels in TC neurons. alpha1A-/-/alpha1G-/- mice showed a complete loss of T-type Ca2+ currents in TC neurons and displayed no SWDs. Interestingly, alpha1A-/-/alpha1G+/- mice had 75% of the T-type Ca2+ currents in TC neurons observed in alpha1A+/+/alpha1G+/+ mice and showed SWD activity that was quantitatively similar to that in alpha1A-/-/alpha1G+/+ mice. Similar results were obtained using double-mutant mice harboring the alpha1G mutation plus another mutation also used as a model for absence seizures, i.e., lethargic (beta4(lh/lh)), tottering (alpha1A(tg/tg)), or stargazer (gamma2(stg/stg)). The present results reveal that alpha1G T-type Ca2+ channels play a critical role in the genesis of spontaneous absence seizures resulting from hypofunctioning P/Q-type channels, but that the augmentation of thalamic T-type Ca2+ currents is not an essential step in the genesis of absence seizures.
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