Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:9070745rdf:typepubmed:Citationlld:pubmed
pubmed-article:9070745lifeskim:mentionsumls-concept:C0010453lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C0007765lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C0596630lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C0015283lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C1704632lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C0871261lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C2911692lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C1706817lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C1527148lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C0596235lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C1948027lld:lifeskim
pubmed-article:9070745lifeskim:mentionsumls-concept:C0439799lld:lifeskim
pubmed-article:9070745pubmed:issue3lld:pubmed
pubmed-article:9070745pubmed:dateCreated1997-6-10lld:pubmed
pubmed-article:9070745pubmed:abstractTextUsing single-cell imaging, we investigated developmental changes in the modulation of KCl-evoked Ca2+ entry by various voltage-dependent Ca2+ channels and the coupling of these channels to exocytosis in cultured cerebellar granule neurons. A component of the KCl-evoked Ca2+ elevation sensitive to nifedipine and localized at cell somata, decreases with culture age. A component blocked by 200 nM omega-Agatoxin-IVA increases with age and whilst localized primarily at the cell somata, also becomes evident at the neurites. The change in activity between nifedipine-sensitive Ca2+ channels and omega-Agatoxin-IVA-sensitive Ca2+ channels occurs at 13 days in vitro at cell somata. A component of Ca2+ entry insensitive to nifedipine and 200 nM omega-Agatoxin-IVA is localized primarily at the neurites and is apparent at all ages. Single-cell imaging of exocytosis using FM1-43 destaining indicates that the residual, but not the nifedipine- or omega-Agatoxin-IVA-sensitive components of Ca2+ entry, modulates exocytosis. However cells cultured for 20-26 days develop a component of Ca2+ entry at the neurites which is sensitive to 200 nM omega-Agatoxin-IVA and omega-Conotoxin-MVIIC and which partially controls release. Immunolocalization studies reveal that binding sites for omega-Conotoxin-GVIA are present throughout development, even though this toxin does not inhibit KCl-evoked [Ca2+]c elevations or exocytosis. 300 nM omega-Agatoxin-IVA labels both somata and, at later developmental stages, neurites, consistent with the functional studies.lld:pubmed
pubmed-article:9070745pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:languageenglld:pubmed
pubmed-article:9070745pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:citationSubsetIMlld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:9070745pubmed:statusMEDLINElld:pubmed
pubmed-article:9070745pubmed:monthAprlld:pubmed
pubmed-article:9070745pubmed:issn0306-4522lld:pubmed
pubmed-article:9070745pubmed:authorpubmed-author:RitchieJJlld:pubmed
pubmed-article:9070745pubmed:authorpubmed-author:PocockJJlld:pubmed
pubmed-article:9070745pubmed:authorpubmed-author:SmithWWlld:pubmed
pubmed-article:9070745pubmed:authorpubmed-author:NichollsDDlld:pubmed
pubmed-article:9070745pubmed:authorpubmed-author:BowmanDDlld:pubmed
pubmed-article:9070745pubmed:authorpubmed-author:HarroldJJlld:pubmed
pubmed-article:9070745pubmed:issnTypePrintlld:pubmed
pubmed-article:9070745pubmed:volume77lld:pubmed
pubmed-article:9070745pubmed:ownerNLMlld:pubmed
pubmed-article:9070745pubmed:authorsCompleteYlld:pubmed
pubmed-article:9070745pubmed:pagination683-94lld:pubmed
pubmed-article:9070745pubmed:dateRevised2009-9-29lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:meshHeadingpubmed-meshheading:9070745-...lld:pubmed
pubmed-article:9070745pubmed:year1997lld:pubmed
pubmed-article:9070745pubmed:articleTitleThe development of Ca2+ channel responses and their coupling to exocytosis in cultured cerebellar granule cells.lld:pubmed
pubmed-article:9070745pubmed:affiliationNeurosciences Institute, Department of Pharmacology, University of Dundee, U.K.lld:pubmed
pubmed-article:9070745pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9070745pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed