Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:21482359rdf:typepubmed:Citationlld:pubmed
pubmed-article:21482359lifeskim:mentionsumls-concept:C0039729lld:lifeskim
pubmed-article:21482359lifeskim:mentionsumls-concept:C0012621lld:lifeskim
pubmed-article:21482359lifeskim:mentionsumls-concept:C0014553lld:lifeskim
pubmed-article:21482359lifeskim:mentionsumls-concept:C1413059lld:lifeskim
pubmed-article:21482359lifeskim:mentionsumls-concept:C0439799lld:lifeskim
pubmed-article:21482359lifeskim:mentionsumls-concept:C1511545lld:lifeskim
pubmed-article:21482359pubmed:issue1lld:pubmed
pubmed-article:21482359pubmed:dateCreated2011-4-12lld:pubmed
pubmed-article:21482359pubmed:abstractTextNeurons of the reticular thalamus (RT) display oscillatory burst discharges that are believed to be critical for thalamocortical network oscillations related to absence epilepsy. Ca²+-dependent mechanisms underlie such oscillatory discharges. However, involvement of high-voltage activated (HVA) Ca²+ channels in this process has been discounted. We examined this issue closely using mice deficient for the HVA Ca(v)2.3 channels. In brain slices of Ca(v)2.3?/?, a hyperpolarizing current injection initiated a low-threshold burst of spikes in RT neurons; however, subsequent oscillatory burst discharges were severely suppressed, with a significantly reduced slow afterhyperpolarization (AHP). Consequently, the lack of Ca(v)2.3 resulted in a marked decrease in the sensitivity of the animal to ?-butyrolactone-induced absence epilepsy. Local blockade of Ca(v)2.3 channels in the RT mimicked the results of Ca(v)2.3?/? mice. These results provide strong evidence that Ca(v)2.3 channels are critical for oscillatory burst discharges in RT neurons and for the expression of absence epilepsy.lld:pubmed
pubmed-article:21482359pubmed:languageenglld:pubmed
pubmed-article:21482359pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21482359pubmed:citationSubsetIMlld:pubmed
pubmed-article:21482359pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21482359pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21482359pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21482359pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21482359pubmed:statusMEDLINElld:pubmed
pubmed-article:21482359pubmed:monthAprlld:pubmed
pubmed-article:21482359pubmed:issn1097-4199lld:pubmed
pubmed-article:21482359pubmed:authorpubmed-author:ShinHee-SupHSlld:pubmed
pubmed-article:21482359pubmed:authorpubmed-author:LeeC JustinCJlld:pubmed
pubmed-article:21482359pubmed:authorpubmed-author:ChoiJee...lld:pubmed
pubmed-article:21482359pubmed:authorpubmed-author:CheongEunjiElld:pubmed
pubmed-article:21482359pubmed:authorpubmed-author:ZamanTariqTlld:pubmed
pubmed-article:21482359pubmed:authorpubmed-author:PaydarAfshinAlld:pubmed
pubmed-article:21482359pubmed:authorpubmed-author:LeeKyoobinKlld:pubmed
pubmed-article:21482359pubmed:authorpubmed-author:ParkCheongdah...lld:pubmed
pubmed-article:21482359pubmed:copyrightInfoCopyright © 2011 Elsevier Inc. All rights reserved.lld:pubmed
pubmed-article:21482359pubmed:issnTypeElectroniclld:pubmed
pubmed-article:21482359pubmed:day14lld:pubmed
pubmed-article:21482359pubmed:volume70lld:pubmed
pubmed-article:21482359pubmed:ownerNLMlld:pubmed
pubmed-article:21482359pubmed:authorsCompleteYlld:pubmed
pubmed-article:21482359pubmed:pagination95-108lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:meshHeadingpubmed-meshheading:21482359...lld:pubmed
pubmed-article:21482359pubmed:year2011lld:pubmed
pubmed-article:21482359pubmed:articleTitleCav2.3 channels are critical for oscillatory burst discharges in the reticular thalamus and absence epilepsy.lld:pubmed
pubmed-article:21482359pubmed:affiliationCenter for Neural Science, Korea Institute of Science and Technology (KIST), Seoul 136-791, Korea.lld:pubmed
pubmed-article:21482359pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21482359pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:21482359pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
entrez-gene:777entrezgene:pubmedpubmed-article:21482359lld:entrezgene
entrez-gene:12290entrezgene:pubmedpubmed-article:21482359lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:21482359lld:entrezgene