ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Mutations in high-voltage-activated calcium channel genes stimulate low-voltage-activated currents in mouse thalamic relay neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 2 of them syntheses that pooled it.
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Who cites it
93 citing papers in PubMed, 2 syntheses or guidelines pooled it, 194 citations in OpenAlex.
- Analysing an allelic series of rare missense variants of CACNA1I in a Swedish schizophrenia cohort.Brain : a journal of neurology · 2022Pooled it
- Genetic associations between voltage-gated calcium channels and autism spectrum disorder: a systematic review.Molecular brain · 2020Pooled it
- Convergent Inhibitory Cortical Circuit Disruption Drives Genetically Distinct Absence Seizures.bioRxiv : the preprint server for biology · 2026Article
- Parvalbumin interneuron activation rescues both seizures and impaired social novelty in digenic absence epilepsy mice.Science advances · 2026Article
- Centrally Acting Skeletal Muscle Relaxants Sharing Molecular Targets with Drugs for Neuropathic Pain Management.Brain sciences · 2025Review
- Genetic Animal Models of Idiopathic Generalized Epilepsies: What Can We Learn from Them?Biomedicines · 2025Review
- Review
- Voltage-gated calcium channels in genetic epilepsies.Journal of neurochemistry · 2024Review
- AARS and CACNA1A mutations: diagnostic insights into a case report of uncommon epileptic encephalopathy phenotypes in two siblings.Frontiers in neurology · 2024Article
- Thalamocortical circuits in generalized epilepsy: Pathophysiologic mechanisms and therapeutic targets.Neurobiology of disease · 2023Review
- CaHandbook of experimental pharmacology · 2023Article
- β subunits of voltage-gated calcium channels in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Case Report: A Novel CACNA1A Mutation Caused Flunarizine-Responsive Type 2 Episodic Ataxia and Hemiplegic Migraine With Abnormal MRI of Cerebral White Matter.Frontiers in neurology · 2022Article
- Clinical and molecular spectrum of P/Q type calcium channel Cav2.1 in epileptic patients.Orphanet journal of rare diseases · 2021Article
- 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
- Neuromedin B receptor stimulation of Cav3.2 T-type CaTheranostics · 2021Article
- Global genetic deletion of CaScientific reports · 2020Article
- Neuronal Cav3 channelopathies: recent progress and perspectives.Pflugers Archiv : European journal of physiology · 2020Review
- Genetic T-type calcium channelopathies.Journal of medical genetics · 2020Review
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Ca2+ currents, especially those activated at low voltages (LVA), influence burst generation in thalamocortical circuitry and enhance the abnormal rhythmicity associated with absence epilepsy. Mutations in several genes for high-voltage-activated (HVA) Ca2+ channel subunits are linked to spike-wave seizure phenotypes in mice; however, none of these mutations are predicted to increase intrinsic membrane excitability or directly enhance LVA currents. We examined biophysical properties of both LVA and HVA Ca2+ currents in thalamic cells of tottering (tg; Cav2.1/alpha1A subunit), lethargic (lh; beta4 subunit), and stargazer (stg; gamma2 subunit) brain slices. We observed 46, 51, and 45% increases in peak current densities of LVA Ca2+ currents evoked at -50 mV from -110 mV in tg, lh, and stg mice, respectively, compared with wild type. The half-maximal voltages for steady-state inactivation of LVA currents were shifted in a depolarized direction by 7.5-13.5 mV in all three mutants, although no alterations in the time-constant for recovery from inactivation of LVA currents were found. HVA peak current densities in tg and stg were increased by 22 and 45%, respectively, and a 5 mV depolarizing shift of the activation curve was observed in lh. Despite elevated LVA amplitudes, no alterations in mRNA expression of the genes mediating T-type subunits, Cav3.1/alpha1G, Cav3.2/alpha1H, or Cav3.3/alpha1I, were detected in the three mutants. Our data demonstrate that mutation of Cav2.1 or regulatory subunit genes increases intrinsic membrane excitability in thalamic neurons by potentiating LVA Ca2+ currents. These alterations increase the probability for abnormal thalamocortical synchronization and absence epilepsy in tg, lh, and stg mice.
Indexed as
Identifiers
12151514PMC6758149W2120176125What OpenQuestion holds
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.