Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:10670441rdf:typepubmed:Citationlld:pubmed
pubmed-article:10670441lifeskim:mentionsumls-concept:C0027882lld:lifeskim
pubmed-article:10670441lifeskim:mentionsumls-concept:C0596235lld:lifeskim
pubmed-article:10670441lifeskim:mentionsumls-concept:C1515877lld:lifeskim
pubmed-article:10670441lifeskim:mentionsumls-concept:C0439799lld:lifeskim
pubmed-article:10670441lifeskim:mentionsumls-concept:C0521116lld:lifeskim
pubmed-article:10670441lifeskim:mentionsumls-concept:C1879547lld:lifeskim
pubmed-article:10670441lifeskim:mentionsumls-concept:C0851827lld:lifeskim
pubmed-article:10670441lifeskim:mentionsumls-concept:C1701901lld:lifeskim
pubmed-article:10670441pubmed:issue3lld:pubmed
pubmed-article:10670441pubmed:dateCreated2000-3-1lld:pubmed
pubmed-article:10670441pubmed:abstractTextIt is demonstrated that not all voltage-gated calcium channel types expressed in neostriatal projection neurons (L, N, P, Q and R) contribute equally to the activation of calcium-dependent potassium currents. Previous work made clear that different calcium channel types contribute with a similar amount of current to whole-cell calcium current in neostriatal neurons. It has also been shown that spiny neurons possess both "big" and "small" types of calcium-dependent potassium currents and that activation of such currents relies on calcium entry through voltage-gated calcium channels. In the present work it was investigated whether all calcium channel types equally activate calcium-dependent potassium currents. Thus, the action of organic calcium channel antagonists was investigated on the calcium-activated outward current. Transient potassium currents were reduced by 4-aminopyridine and sodium currents were blocked by tetrodotoxin. It was found that neither 30 nM omega-Agatoxin-TK, a blocker of P-type channels, nor 200 nM calciseptine or 5 microM nitrendipine, blockers of L-type channels, were able to significantly reduce the outward current. In contrast, 400 nM omega-Agatoxin-TK, which at this concentration is able to block Q-type channels, and 1 microM omega-Conotoxin GVIA, a blocker of N-type channels, both reduced outward current by about 50%. These antagonists given together, or 500 nM omega-Conotoxin MVIIC, a blocker of N- and P/Q-type channels, reduced outward current by 70%. In addition, the N- and P/Q-type channel blockers preferentially reduce the afterhyperpolarization recorded intracellularly. The results show that calcium-dependent potassium channels in neostriatal neurons are preferentially activated by calcium entry through N- and Q-type channels in these conditions.lld:pubmed
pubmed-article:10670441pubmed:languageenglld:pubmed
pubmed-article:10670441pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10670441pubmed:citationSubsetIMlld:pubmed
pubmed-article:10670441pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10670441pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10670441pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10670441pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10670441pubmed:statusMEDLINElld:pubmed
pubmed-article:10670441pubmed:issn0306-4522lld:pubmed
pubmed-article:10670441pubmed:authorpubmed-author:GalarragaEElld:pubmed
pubmed-article:10670441pubmed:authorpubmed-author:BargasJJlld:pubmed
pubmed-article:10670441pubmed:authorpubmed-author:GalvánEElld:pubmed
pubmed-article:10670441pubmed:authorpubmed-author:VilchisCClld:pubmed
pubmed-article:10670441pubmed:authorpubmed-author:AyalaG XGXlld:pubmed
pubmed-article:10670441pubmed:issnTypePrintlld:pubmed
pubmed-article:10670441pubmed:volume95lld:pubmed
pubmed-article:10670441pubmed:ownerNLMlld:pubmed
pubmed-article:10670441pubmed:authorsCompleteYlld:pubmed
pubmed-article:10670441pubmed:pagination745-52lld:pubmed
pubmed-article:10670441pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:meshHeadingpubmed-meshheading:10670441...lld:pubmed
pubmed-article:10670441pubmed:year2000lld:pubmed
pubmed-article:10670441pubmed:articleTitleCa2+ channels that activate Ca2+-dependent K+ currents in neostriatal neurons.lld:pubmed
pubmed-article:10670441pubmed:affiliationInstituto de Fisiología Celular, UNAM, México City, DF, México.lld:pubmed
pubmed-article:10670441pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10670441pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10670441lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10670441lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10670441lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10670441lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10670441lld:pubmed