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Article

CaV3.2 calcium channels control NMDA receptor-mediated transmission: a new mechanism for absence epilepsy.

Genes & development - 15 Jul 2015

Wang Guangfu, Bochorishvili Genrieta, Chen Yucai, Salvati Kathryn A, Zhang Peng, Dubel Steve J, Perez-Reyes Edward, Snutch Terrance P, Stornetta Ruth L, Deisseroth Karl, Erisir Alev, Todorovic Slobodan M, Luo Jian-Hong, Kapur Jaideep, Beenhakker Mark P, Zhu J Julius

Abstract excerpt

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...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 26220996
DOI: 10.1101/gad.260869.115
PMCID: PMC4526737

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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