Source:http://linkedlifedata.com/resource/pubmed/id/11133355
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2001-1-26
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| pubmed:abstractText |
Two potential mechanisms by which the intracellular Ca(2 stores might modulate catecholamine release from bovine adrenal chromaffin cells were investigated: (i) that the cytosolic Ca(2+)transient caused by Ca(2+)release from the intracellular stores recruits additional chromaffin granules to a readily releasable pool that results in augmented catecholamine release when this is subsequently evoked, and (ii) that the Ca(2+)influx that follows depletion of intracellular stores (i.e. store-operated Ca(2+)entry) triggers release per se thereby augmenting evoked catecholamine release. When histamine or caffeine were applied in Ca(2+)-free perfusion media, a transient elevation of intracellular free Ca(2+)occurred owing to mobilization of Ca(2+)from the stores. When Ca(2+)was later readmitted to the perfusing fluid there followed a prompt and maintained rise in intracellular Ca(2+)concentrations of magnitude related to the degree of store mobilization. In parallel experiments, increased catecholamine secretion was measured under the conditions when Ca(2+)influx following store-mobilization occurred. Furthermore, the size of the catecholamine release increment correlated with the degree of Ca(2+)influx. Store-operated Ca(2+)entry evoked by mobilization with histamine and/or caffeine did not augment nicotine-evoked secretion per se; that is, it augmented evoked catecholamine release only to the extent that it increased basal catecholamine release. The nicotine-evoked catecholamine release was sensitive to cytosolic BAPTA, which, at the concentration used (50 microM BAPTA-AM), reduced release by approximately 25%. However, the increment in basal catecholamine release which followed Ca(2+)influx triggered by Ca(2+)store mobilization was not reduced by intracellular BAPTA. This finding is inconsistent with the hypothesis that the elevated cytosolic Ca(2+)from store mobilization recruits additional vesicles of catecholamine to the sub-plasmalemmal release sites to augment subsequently evoked secretion. This position is supported by the observation that histamine (10 microM) in Ca(2+)-free medium caused a pronounced elevation of cytosolic free Ca(2+), but this caused no greater catecholamine release when Ca(2+)was re-introduced than did prior exposure to Ca(2+)-free medium alone, which caused no elevation of cytosolic free Ca(2+). It is concluded that intracellular Ca(2+)stores can modulate secretion of catecholamines from bovine chromaffin cells by permitting Ca(2+)influx through a store-operated entry pathway. The results do not support the notion that the Ca(2+)released from intracellular stores plays a significant role in the recruitment of vesicles into the ready-release pool under the experimental conditions reported here.
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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/1,2-bis(2-aminophenoxy)ethane-N,N,N'...,
http://linkedlifedata.com/resource/pubmed/chemical/Caffeine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Chelating Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Epinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorescent Dyes,
http://linkedlifedata.com/resource/pubmed/chemical/Fura-2,
http://linkedlifedata.com/resource/pubmed/chemical/Histamine,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphodiesterase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nicotinic
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0143-4160
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2001 Harcourt Publishers Ltd.
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| pubmed:issnType |
Print
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| pubmed:volume |
29
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
49-58
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:11133355-Adrenal Medulla,
pubmed-meshheading:11133355-Animals,
pubmed-meshheading:11133355-Caffeine,
pubmed-meshheading:11133355-Calcium,
pubmed-meshheading:11133355-Cattle,
pubmed-meshheading:11133355-Cells, Cultured,
pubmed-meshheading:11133355-Chelating Agents,
pubmed-meshheading:11133355-Chromaffin Cells,
pubmed-meshheading:11133355-Cytosol,
pubmed-meshheading:11133355-Egtazic Acid,
pubmed-meshheading:11133355-Epinephrine,
pubmed-meshheading:11133355-Exocytosis,
pubmed-meshheading:11133355-Fluorescent Dyes,
pubmed-meshheading:11133355-Fura-2,
pubmed-meshheading:11133355-Histamine,
pubmed-meshheading:11133355-Norepinephrine,
pubmed-meshheading:11133355-Phosphodiesterase Inhibitors,
pubmed-meshheading:11133355-Receptors, Nicotinic
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| pubmed:year |
2001
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| pubmed:articleTitle |
Neurotransmitter release from bovine adrenal chromaffin cells is modulated by capacitative Ca(2+)entry driven by depleted internal Ca(2+)stores.
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| pubmed:affiliation |
The Neuroscience Group, Faculty of Medicine and Health Sciences, The University of Newcastle, New South Wales, 2308, Australia.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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