Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Altered seizure susceptibility in mice lacking the Ca(v)2.3 E-type Ca2+ channel.

Epilepsia - 1 May 2006

Weiergräber Marco, Henry Margit, Krieger Andreas, Kamp Marcel, Radhakrishnan Kayalvizhi, Hescheler Jürgen, Schneider Toni

Abstract excerpt

PURPOSE: Recently the Ca(v)2.3 (E/R-type) voltage-gated calcium channel (VGCC) has turned out to be not only a potential target for different antiepileptic drugs (e.g., lamotrigine, topiramate) but also a crucial component in the pathogenesis of absence epilepsy, human juvenile myoclonic epilepsy (JME), and epileptiform activity in CA1 neurons. The aim of our study was to perform an electroencephalographic...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Calcium Channels
Share to Calcium Channels, T-Type

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Electroencephalography

Share to Electromyography

Share to Hippocampus

Share to Ion Channel Gating

Share to Pentylenetetrazole

Share to Seizures

Source

Identifiers

PMID: 16686648
DOI: 10.1111/j.1528-1167.2006.00541.x

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.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Altered seizure susceptibility in mice lacking the Ca(v)2.3 E-type Ca2+ channel.PMID 16686648Read ↗

Insights from mouse models of absence epilepsy into Ca2+ channel physiology and disease etiology.Semantic proximity Read ↗

Transcriptional upregulation of Cav3.2 mediates epileptogenesis in the pilocarpine model of epilepsy.Semantic proximity Read ↗

Ca2+ channels and epilepsy.Semantic proximity Read ↗

Cav2.3 (R-Type) Calcium Channels are Critical for Mediating Anticonvulsive and Neuroprotective Properties of Lamotrigine In Vivo.Semantic proximity Read ↗

Kv4.2 knockout mice demonstrate increased susceptibility to convulsant stimulation.Semantic proximity Read ↗

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

Cortical alterations in a model for absence epilepsy and febrile seizures: in vivo findings in mice carrying a human GABA(A)R gamma2 subunit mutation.Semantic proximity Read ↗

Phenotypic Characterization of Larval Zebrafish (Danio rerio) with Partial Knockdown of the cacna1a Gene.Semantic proximity Read ↗

Mechanisms by which a CACNA1H mutation in epilepsy patients increases seizure susceptibilitySemantic proximity Read ↗

A genetic switch for epilepsy in adult mice.Semantic proximity Read ↗

Effects of Ca<sub>v</sub>3.2 channel mutations linked to idiopathic generalized epilepsySemantic proximity Read ↗

Altered hippocampal activation in seizure-prone <i>CACNA2D2</i> knockout miceSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.