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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2000-11-7
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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.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10970427-10048592,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10970427-10393875,
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
527 Pt 2
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
249-64
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10970427-Animals,
pubmed-meshheading:10970427-Calcium,
pubmed-meshheading:10970427-Calcium Channel Blockers,
pubmed-meshheading:10970427-Calcium Channels, N-Type,
pubmed-meshheading:10970427-Chloride Channels,
pubmed-meshheading:10970427-Electrophysiology,
pubmed-meshheading:10970427-Male,
pubmed-meshheading:10970427-Membrane Potentials,
pubmed-meshheading:10970427-Mice,
pubmed-meshheading:10970427-Neurons,
pubmed-meshheading:10970427-Nifedipine,
pubmed-meshheading:10970427-Potassium Channels,
pubmed-meshheading:10970427-Rats,
pubmed-meshheading:10970427-Ryanodine,
pubmed-meshheading:10970427-Superior Cervical Ganglion,
pubmed-meshheading:10970427-Sympathetic Nervous System,
pubmed-meshheading:10970427-omega-Agatoxin IVA,
pubmed-meshheading:10970427-omega-Conotoxin GVIA
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pubmed:year |
2000
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pubmed:articleTitle |
Distinct mechanisms for activation of Cl- and K+ currents by Ca2+ from different sources in mouse sympathetic neurones.
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pubmed:affiliation |
Instituto de Neurociencias, Universidad Miguel Hernández-CSIC, Apartado 18, 03550 San Juan de Alicante, Spain.
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pubmed:publicationType |
Journal Article
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