ArticleThe Journal of physiology2002
Specific contribution of human T-type calcium channel isotypes (alpha(1G), alpha(1H) and alpha(1I)) to neuronal excitability.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 223 citations in OpenAlex.
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- Activation of GABA transmission by clonazepam reverses the autistic-like phenotypes of the Cav3.2 knockout mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Muscarinic Receptor Activation Preferentially Inhibits Rebound in Vulnerable Dopaminergic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
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- Muscarinic receptor activation preferentially inhibits rebound in vulnerable dopaminergic neurons.bioRxiv : the preprint server for biology · 2024Article
- Genomic evidence for the suitability of Göttingen Minipigs with a rare seizure phenotype as a model for human epilepsy.Neurogenetics · 2024Article
- Pathophysiology of ion channels in amyotrophic lateral sclerosis.Molecular brain · 2023Review
- T-type CaCell reports · 2023Article
- Whole Exome Sequencing of Hemiplegic Migraine Patients Shows an Increased Burden of Missense Variants in CACNA1H and CACNA1I Genes.Molecular neurobiology · 2023Article
- Review
- Effects of progesterone on T-type-CaNeural regeneration research · 2022Article
- Circuits and components of delta wave regulation.Brain research bulletin · 2022Review
- Neocortical localization and thalamocortical modulation of neuronal hyperexcitability contribute to Fragile X Syndrome.Communications biology · 2022Article
- Central and peripheral contributions of T-type calcium channels in pain.Molecular brain · 2022Review
- Modulation of Recombinant Human T-Type Calcium Channels by ΔCannabis and cannabinoid research · 2022Article
- Painful diabetic neuropathy leads to functional CaExperimental neurology · 2021Article
48 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In several types of neurons, firing is an intrinsic property produced by specific classes of ion channels. Low-voltage-activated T-type calcium channels (T-channels), which activate with small membrane depolarizations, can generate burst firing and pacemaker activity. Here we have investigated the specific contribution to neuronal excitability of cloned human T-channel subunits. Using HEK-293 cells transiently transfected with the human alpha(1G) (Ca(V)3.1), alpha(1H) (Ca(V)3.2) and alpha(1I) (Ca(V)3.3) subunits, we describe significant differences among these isotypes in their biophysical properties, which are highlighted in action potential clamp studies. Firing activities occurring in cerebellar Purkinje neurons and in thalamocortical relay neurons used as voltage clamp waveforms revealed that alpha(1G) channels and, to a lesser extent, alpha(1H) channels produced large and transient currents, while currents related to alpha(1I) channels exhibited facilitation and produced a sustained calcium entry associated with the depolarizing after-potential interval. Using simulations of reticular and relay thalamic neuron activities, we show that alpha(1I) currents contributed to sustained electrical activities, while alpha(1G) and alpha(1H) currents generated short burst firing. Modelling experiments with the NEURON model further revealed that the alpha(1G) channel and alpha(1I) channel parameters best accounted for T-channel activities described in thalamocortical relay neurons and in reticular neurons, respectively. Altogether, the data provide evidence for a role of alpha(1I) channel in pacemaker activity and further demonstrate that each T-channel pore-forming subunit displays specific gating properties that account for its unique contribution to neuronal firing.
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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.