pubmed-article:10970427 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10970427 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:10970427 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:10970427 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
pubmed-article:10970427 | lifeskim:mentions | umls-concept:C0596019 | lld:lifeskim |
pubmed-article:10970427 | lifeskim:mentions | umls-concept:C0449416 | lld:lifeskim |
pubmed-article:10970427 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:10970427 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
pubmed-article:10970427 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:10970427 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:10970427 | pubmed:dateCreated | 2000-11-7 | lld:pubmed |
pubmed-article:10970427 | pubmed:abstractText | We have investigated the roles of different voltage-dependent Ca2+ channels in the activation of the Cl- and K+ channels responsible for the afterdepolarization (ADP) and slow afterhyperpolarization (AHP) in sympathetic neurones of the isolated mouse superior cervical ganglion in vitro. The ADP and its associated Ca2+-activated Cl- current were markedly decreased by omega-agatoxin IVA (40-200 nM) and nifedipine (1-10 microM), but not by omega-conotoxin GVIA (300 nM). In contrast, the AHP and the apamin-sensitive Ca2+-activated K+ current that underlies this potential were blocked by omega-conotoxin GVIA, but were not affected by omega-agatoxin IVA and were only slightly reduced by nifedipine. Ryanodine (20 microM) reduced the Ca2+-activated Cl- current following an action potential by 75% but on average did not affect the Ca2+-activated K+ current. Evidence that R-type channels provide a proportion of the Ca2+ activating both types of Ca2+-dependent channel was obtained. We conclude that Ca2+ entering through L- and P-type Ca2+ channels preferentially activates the Cl- current responsible for the ADP in mouse sympathetic neurones, predominantly via Ca2+-induced Ca2+ release, whereas the Ca2+ that activates the K+ channels responsible for the AHP enters predominantly through N-type channels. The data can be explained by the selective association of each type of Ca2+ channel with particular intracellular mechanisms for activating other membrane channels, one indirect and the other direct, probably located at discrete sites on the soma and dendrites. | lld:pubmed |
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pubmed-article:10970427 | pubmed:language | eng | lld:pubmed |
pubmed-article:10970427 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10970427 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10970427 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10970427 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10970427 | pubmed:month | Sep | lld:pubmed |
pubmed-article:10970427 | pubmed:issn | 0022-3751 | lld:pubmed |
pubmed-article:10970427 | pubmed:author | pubmed-author:McLachlanE... | lld:pubmed |
pubmed-article:10970427 | pubmed:author | pubmed-author:GallegoRR | lld:pubmed |
pubmed-article:10970427 | pubmed:author | pubmed-author:Martínez-Pinn... | lld:pubmed |
pubmed-article:10970427 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10970427 | pubmed:day | 1 | lld:pubmed |
pubmed-article:10970427 | pubmed:volume | 527 Pt 2 | lld:pubmed |
pubmed-article:10970427 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10970427 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10970427 | pubmed:pagination | 249-64 | lld:pubmed |
pubmed-article:10970427 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:10970427 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10970427 | pubmed:articleTitle | Distinct mechanisms for activation of Cl- and K+ currents by Ca2+ from different sources in mouse sympathetic neurones. | lld:pubmed |
pubmed-article:10970427 | pubmed:affiliation | Instituto de Neurociencias, Universidad Miguel Hernández-CSIC, Apartado 18, 03550 San Juan de Alicante, Spain. | lld:pubmed |
pubmed-article:10970427 | pubmed:publicationType | Journal Article | lld:pubmed |