pubmed-article:8985597 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8985597 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
pubmed-article:8985597 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:8985597 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:8985597 | lifeskim:mentions | umls-concept:C1708248 | lld:lifeskim |
pubmed-article:8985597 | lifeskim:mentions | umls-concept:C0026237 | lld:lifeskim |
pubmed-article:8985597 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
pubmed-article:8985597 | lifeskim:mentions | umls-concept:C0443301 | lld:lifeskim |
pubmed-article:8985597 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:8985597 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:8985597 | pubmed:dateCreated | 1997-3-18 | lld:pubmed |
pubmed-article:8985597 | pubmed:abstractText | Intracellular Ca2+ ([Ca2+]i) dynamics were studied in identified rat gonadotropes using the whole-cell patch-clamp technique in conjunction with Indo-1 photometry. The kinetics of depolarization-induced [Ca2+]i transients vary with Ca2+ load. In addition to a rapid initial decay, large (> 500 nM) [Ca2+]i transients have a slow plateau phase. Application of the mitochondrial inhibitor carbonyl cyanide m-chlorophenylhydrazone (CCCP) significantly slows the decay of [Ca2+]i transients, consistent with stopping uptake of Ca2+ by mitochondria. CCCP causes a small increase of [Ca2+]i at rest. After a large Ca2+ entry the amount is much larger, consistent with release from a mitochondrial Ca2+ pool that fills during cytoplasmic Ca2+ loading. The rate of Ca2+ uptake by mitochondria is dependent upon [Ca2+]i. Consistent with previous studies, gonadotropin releasing hormone (GnRH) induces [Ca2+]i oscillations. The mitochondrial inhibitors CCCP and cyanide (CN-) terminate these oscillations. The mitochondrial ATP-synthase inhibitor oligomycin reduces the frequency and increases the amplitude of the oscillations. In the presence of ruthenium red (a non-specific blocker of the mitochondrial Ca(2+)-uniporter) in the pipette, GnRH does not induce rhythmic [Ca2+]i oscillations. We suggest that mitochondria play a significant role in the rapid clearance of cytosolic Ca2+ loads in gonadotropes and participate in GnRH-induced periodic [Ca2+]i oscillations. | lld:pubmed |
pubmed-article:8985597 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8985597 | pubmed:language | eng | lld:pubmed |
pubmed-article:8985597 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8985597 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:8985597 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8985597 | pubmed:month | Dec | lld:pubmed |
pubmed-article:8985597 | pubmed:issn | 0143-4160 | lld:pubmed |
pubmed-article:8985597 | pubmed:author | pubmed-author:HilleBB | lld:pubmed |
pubmed-article:8985597 | pubmed:author | pubmed-author:HeikMM | lld:pubmed |
pubmed-article:8985597 | pubmed:author | pubmed-author:GolardAA | lld:pubmed |
pubmed-article:8985597 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8985597 | pubmed:volume | 20 | lld:pubmed |
pubmed-article:8985597 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8985597 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8985597 | pubmed:pagination | 515-24 | lld:pubmed |
pubmed-article:8985597 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:8985597 | pubmed:year | 1996 | lld:pubmed |
pubmed-article:8985597 | pubmed:articleTitle | Involvement of mitochondria in intracellular calcium sequestration by rat gonadotropes. | lld:pubmed |
pubmed-article:8985597 | pubmed:affiliation | Department of Physiology and Biophysics, University of Washington, Seattle 98195-7290, USA. | lld:pubmed |
pubmed-article:8985597 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8985597 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:8985597 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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