pubmed-article:10330407 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0007776 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0022655 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0001613 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0004112 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0026237 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0015264 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0678544 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0205160 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0015744 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C2911691 | lld:lifeskim |
pubmed-article:10330407 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:10330407 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:10330407 | pubmed:dateCreated | 1999-7-21 | lld:pubmed |
pubmed-article:10330407 | pubmed:abstractText | We have used digital fluorescence imaging techniques to explore the interplay between mitochondrial Ca2+ uptake and physiological Ca2+ signaling in rat cortical astrocytes. A rise in cytosolic Ca2+ ([Ca2+]cyt), resulting from mobilization of ER Ca2+ stores was followed by a rise in mitochondrial Ca2+ ([Ca2+]m, monitored using rhod-2). Whereas [Ca2+]cyt recovered within approximately 1 min, the time to recovery for [Ca2+]m was approximately 30 min. Dissipating the mitochondrial membrane potential (Deltapsim, using the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxy-phenyl-hydrazone [FCCP] with oligomycin) prevented mitochondrial Ca2+ uptake and slowed the rate of decay of [Ca2+]cyt transients, suggesting that mitochondrial Ca2+ uptake plays a significant role in the clearance of physiological [Ca2+]cyt loads in astrocytes. Ca2+ signals in these cells initiated either by receptor-mediated ER Ca2+ release or mechanical stimulation often consisted of propagating waves (measured using fluo-3). In response to either stimulus, the wave traveled at a mean speed of 22.9 +/- 11.2 micrometer/s (n = 262). This was followed by a wave of mitochondrial depolarization (measured using tetramethylrhodamine ethyl ester [TMRE]), consistent with Ca2+ uptake into mitochondria as the Ca2+ wave traveled across the cell. Collapse of Deltapsim to prevent mitochondrial Ca2+ uptake significantly increased the rate of propagation of the Ca2+ waves by 50%. Taken together, these data suggest that cytosolic Ca2+ buffering by mitochondria provides a potent mechanism to regulate the localized spread of astrocytic Ca2+ signals. | lld:pubmed |
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pubmed-article:10330407 | pubmed:language | eng | lld:pubmed |
pubmed-article:10330407 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10330407 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10330407 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10330407 | pubmed:status | MEDLINE | lld:pubmed |