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Article

The I-II loop controls plasma membrane expression and gating of Ca(v)3.2 T-type Ca2+ channels: a paradigm for childhood absence epilepsy mutations.

The Journal of neuroscience : the official journal of the Society for Neuroscience - 10 Jan 2007

Vitko Iuliia, Bidaud Isabelle, Arias Juan Manuel, Mezghrani Alexandre, Lory Philippe, Perez-Reyes Edward

Abstract excerpt

Calcium currents via low-voltage-activated T-type channels mediate burst firing, particularly in thalamic neurons. Considerable evidence supports the hypothesis that overactive T-channels may contribute to thalamocortical dysrhythmia, including absence epilepsy. Single nucleotide polymorphisms in one of the T-channel genes (CACNA1H, which encodes Ca(v)3.2) are associated with childhood absence epilepsy in a...

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Share to Calcium Channels, T-Type
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Epilepsy, Absence

Share to Intracellular Fluid

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Share to Membrane Potentials

Share to Repetitive Sequences, Amino Acid

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Source

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Identifiers

PMID: 17215393
DOI: 10.1523/JNEUROSCI.1817-06.2007
PMCID: PMC6672065

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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The I-II loop controls plasma membrane expression and gating of Ca(v)3.2 T-type Ca2+ channels: a paradigm for childhood absence epilepsy mutations.PMID 17215393Read ↗

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