ArticleGenes & development2015
CaV3.2 calcium channels control NMDA receptor-mediated transmission: a new mechanism for absence epilepsy.
Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Gene discovery and polygenic prediction from a genome-wide association study of educational attainment in 1.1 million individuals.Nature genetics · 2018Pooled it
- Cannabidiol dose modulates behavioral response to acute and repeated administration of Δ9-Tetrahydrocannabinol by strain and sex.bioRxiv : the preprint server for biology · 2026Article
- Impact of Oxidative Stress and Neuroinflammation on Sarco/Endoplasmic Reticulum CaACS pharmacology & translational science · 2025Article
- Calcium- and calmodulin-dependent inhibition of NMDA receptor currents.Biophysical journal · 2024Review
- Article
- Regulation of specific abnormal calcium signals in the hippocampal CA1 and primary cortex M1 alleviates the progression of temporal lobe epilepsy.Neural regeneration research · 2024Article
- T-type calcium channels as therapeutic targets in essential tremor and Parkinson's disease.Annals of clinical and translational neurology · 2023Review
- Genetic mechanisms in generalized epilepsies.Acta epileptologica · 2023Review
- Cav3.1-driven bursting firing in ventromedial hypothalamic neurons exerts dual control of anxiety-like behavior and energy expenditure.Molecular psychiatry · 2022Article
- Invertebrate neurons as a simple model to study the hyperexcitable state of epileptic disorders in single cells, monosynaptic connections, and polysynaptic circuits.Biophysical reviews · 2022Review
- The T-Type Calcium Channel Cav3.2 in Somatostatin Interneurons in Spinal Dorsal Horn Participates in Mechanosensation and Mechanical Allodynia in Mice.Frontiers in cellular neuroscience · 2022Article
- FXR1 regulation of parvalbumin interneurons in the prefrontal cortex is critical for schizophrenia-like behaviors.Molecular psychiatry · 2021Article
- The Property-Based Practical Applications and Solutions of Genetically Encoded Acetylcholine and Monoamine Sensors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures.Brain : a journal of neurology · 2020Review
- Effects of repetitive Iodine thyroid blocking on the foetal brain and thyroid in rats: a systems biology approach.Scientific reports · 2020Article
- A rare CACNA1H variant associated with amyotrophic lateral sclerosis causes complete loss of CaMolecular brain · 2020Article
- Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms.Brain : a journal of neurology · 2020Article
- Cav3.2 calcium channel interactions with the epithelial sodium channel ENaC.Molecular brain · 2019Article
- Out of thin air: Hyperventilation-triggered seizures.Brain research · 2019Review
- Effects of the T-type calcium channel antagonist Z944 on paired associates learning and locomotor activity in rats treated with the NMDA receptor antagonist MK-801.Psychopharmacology · 2018Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 4 countries.
Funding
Abstract
CaV3.2 T-type calcium channels, encoded by CACNA1H, are expressed throughout the brain, yet their general function remains unclear. We discovered that CaV3.2 channels control NMDA-sensitive glutamatergic receptor (NMDA-R)-mediated transmission and subsequent NMDA-R-dependent plasticity of AMPA-R-mediated transmission at rat central synapses. Interestingly, functional CaV3.2 channels primarily incorporate into synapses, replace existing CaV3.2 channels, and can induce local calcium influx to control NMDA transmission strength in an activity-dependent manner. Moreover, human childhood absence epilepsy (CAE)-linked hCaV3.2(C456S) mutant channels have a higher channel open probability, induce more calcium influx, and enhance glutamatergic transmission. Remarkably, cortical expression of hCaV3.2(C456S) channels in rats induces 2- to 4-Hz spike and wave discharges and absence-like epilepsy characteristic of CAE patients, which can be suppressed by AMPA-R and NMDA-R antagonists but not T-type calcium channel antagonists. These results reveal an unexpected role of CaV3.2 channels in regulating NMDA-R-mediated transmission and a novel epileptogenic mechanism for human CAE.
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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.