Linked Life Data

18834942

Source:http://linkedlifedata.com/resource/pubmed/id/18834942

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2008-11-25
pubmed:abstractText
Voltage-gated calcium channels (VGCCs) are key regulators of neuronal excitability and important factors in epileptogenesis and neurodegeneration. Recent findings suggest a novel, important proictogenic and proneuroapoptotic role of the Ca(v)2.3 E/R-type VGCCs in convulsive generalized tonic-clonic and hippocampal seizures. Though Ca(v)2.3 is also expressed in key structures of the thalamocortical circuitry, their functional relevance in non-convulsive absence seizure activity remains unknown. To this end, we investigated absence specific spike-wave discharge (SWD) susceptibility in control and Ca(v)2.3-deficient mice by systemic administration of gamma-hydroxybutyrolactone (GBL, 70 mg/kg i.p.), followed by electrocorticographic radiotelemetric recordings, behavioral analysis and histomorphological characterization. Based on motoric studies, SWD and power-spectrum density (PSD) analysis, our results demonstrate that Ca(v)2.3(-/-) mice exhibit increased absence seizure susceptibility and altered absence seizure architecture compared to control animals. This study provides evidence for the first time that Ca(v)2.3 E/R-type Ca2+ channels are important in modulating thalamocortical hyperoscillation exerting anti-epileptogenic effects in non-convulsive absence seizures.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1095-9327
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
605-18
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Altered thalamocortical rhythmicity in Ca(v)2.3-deficient mice.
pubmed:affiliation
Institute of Neurophysiology, Faculty of Medicine, University of Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Germany. akp74@uni-koeln.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't