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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
19
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pubmed:dateCreated |
1987-8-14
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pubmed:abstractText |
The existence and mechanisms of inactivation of voltage-gated Ca2+ channels are important, but still debatable, physiological problems. By using the Ca2+ indicators quin2 and fura-2, we demonstrate that in PC12 cells voltage-gated Ca2+ channels undergo inactivation dependent on both voltage and [Ca2+]i. Inactivation, however, is never complete and a small number of channels remains open during prolonged depolarization, explaining the steady state elevation of [Ca2+]i observed in cells depolarized with high KCl. A close parallel exists between Ca2+ channel inactivation and the transient nature of neurotransmitter release: secretion is rapidly stimulated during the first 30 s of depolarization, when a transient overshoot in [Ca2+]i can be demonstrated, while it is negligible during the following period, despite the persistence of an elevated [Ca2+]i; predepolarization in Ca2+-free medium and subsequent addition of Ca2+ (a condition which allows the development of the voltage inactivation) abolishes the fast phase of secretion, while not modifying the steady state [Ca2+]i eventually attained; and increases in the intracellular Ca2+ buffering decreases the amplitude of the fast secretion phase induced by KCl without altering the steady state [Ca2+]i. We suggest that localized [Ca2+]i gradients form close to the plasma membrane shortly after depolarization and that the [Ca2+]i reached in these regions is the relevant parameter in the regulation of secretion.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Aminoquinolines,
http://linkedlifedata.com/resource/pubmed/chemical/Benzofurans,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Fura-2,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotransmitter Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Quin2
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
5
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pubmed:volume |
262
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
9189-95
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2439506-Adrenal Gland Neoplasms,
pubmed-meshheading:2439506-Aminoquinolines,
pubmed-meshheading:2439506-Animals,
pubmed-meshheading:2439506-Benzofurans,
pubmed-meshheading:2439506-Calcium,
pubmed-meshheading:2439506-Dopamine,
pubmed-meshheading:2439506-Fura-2,
pubmed-meshheading:2439506-Ion Channels,
pubmed-meshheading:2439506-Kinetics,
pubmed-meshheading:2439506-Mathematics,
pubmed-meshheading:2439506-Neurotransmitter Agents,
pubmed-meshheading:2439506-Pheochromocytoma,
pubmed-meshheading:2439506-Potassium Chloride,
pubmed-meshheading:2439506-Rats
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pubmed:year |
1987
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pubmed:articleTitle |
Voltage-dependent activation and inactivation of calcium channels in PC12 cells. Correlation with neurotransmitter release.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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