| pubmed-article:11032781 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11032781 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:11032781 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:11032781 | lifeskim:mentions | umls-concept:C0206116 | lld:lifeskim |
| pubmed-article:11032781 | lifeskim:mentions | umls-concept:C0003075 | lld:lifeskim |
| pubmed-article:11032781 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:11032781 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:11032781 | pubmed:dateCreated | 2001-1-26 | lld:pubmed |
| pubmed-article:11032781 | pubmed:abstractText | Recent work from this laboratory has demonstrated that purinergic-mediated depolarization of human microglia inhibited a store-operated pathway for entry of Ca2+. We have used Fura-2 spectrofluorometry to investigate the effects on store-operated Ca2+ influx induced by replacement of NaCl with Na-gluconate in extracellular solutions. Three separate procedures were used to activate store-operated channels. Platelet activating factor (PAF) was used to generate a sustained influx of Ca2+ in standard physiological saline solution (PSS). The magnitude of this response was depressed by 70% after replacement of PSS with low Cl- PSS. A second procedure used ATP, initially applied in Ca2+-free PSS solution to deplete intracellular stores. The subsequent perfusion of PSS solution containing Ca2+ resulted in a large and sustained entry of Ca2+, which was inhibited by 75% with low Cl- PSS. The SERCA inhibitor cyclopiazonic acid (CPA) was used to directly deplete stores in zero-Ca2+ PSS. Following the introduction of PSS containing Ca2+, a maintained stores-operated influx of Ca2+ was evident which was inhibited by 77% in the presence of the low Cl- PSS. Ca2+ influx was linearly reduced with cell depolarization in elevated K+ (7.5 to 35 mM) suggesting that changes in external Cl- were manifest as altered electrical driving force for Ca2+ entry. However, 50 mM external KCl effectively eliminated divalent entry which may indicate inactivation of this pathway with high magnitudes of depolarization. Patch clamp studies showed low Cl-PSS to cause depolarizing shifts in both holding currents and reversal potentials of currents activated with voltage ramps. The results demonstrate that Cl- channels play an important role in regulating store-operated entry of Ca2+ in human microglia. | lld:pubmed |
| pubmed-article:11032781 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11032781 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11032781 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11032781 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11032781 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11032781 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11032781 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11032781 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11032781 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11032781 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11032781 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11032781 | pubmed:issn | 0143-4160 | lld:pubmed |
| pubmed-article:11032781 | pubmed:author | pubmed-author:IGNAEE | lld:pubmed |
| pubmed-article:11032781 | pubmed:author | pubmed-author:KimS USU | lld:pubmed |
| pubmed-article:11032781 | pubmed:author | pubmed-author:NagaiAA | lld:pubmed |
| pubmed-article:11032781 | pubmed:author | pubmed-author:McLarnonJ GJG | lld:pubmed |
| pubmed-article:11032781 | pubmed:author | pubmed-author:ChoiH BHB | lld:pubmed |
| pubmed-article:11032781 | pubmed:author | pubmed-author:GoghariVV | lld:pubmed |
| pubmed-article:11032781 | pubmed:author | pubmed-author:FranciosiSS | lld:pubmed |
| pubmed-article:11032781 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11032781 | pubmed:volume | 28 | lld:pubmed |
| pubmed-article:11032781 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11032781 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11032781 | pubmed:pagination | 261-8 | lld:pubmed |
| pubmed-article:11032781 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:11032781 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11032781 | pubmed:articleTitle | Anion channels modulate store-operated calcium influx in human microglia. | lld:pubmed |
| pubmed-article:11032781 | pubmed:affiliation | Department of Pharmacology and Therapeutics, Faculty of Medicine, The University of British Columbia, Vancouver, British Columbia, Canada. Mclarnon@interchange.ubc.ca | lld:pubmed |
| pubmed-article:11032781 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11032781 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:11032781 | lld:pubmed |
