| pubmed-article:11841577 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0521119 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0596902 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0439064 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C1707723 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0205250 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:11841577 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:11841577 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:11841577 | pubmed:dateCreated | 2002-2-13 | lld:pubmed |
| pubmed-article:11841577 | pubmed:abstractText | The release of [3H]GABA evoked by depolarization with various concentrations of KCl was studied using superfused rat cerebrocortex synaptosomes. Elevating [K+] produced release of [3H]GABA over basal which was increasingly less dependent on external Ca2+ but more sensitive to the GABA transporter blocker SKF 100330 A. Accordingly, the sensitivity to clostridial toxins of the depolarization-evoked amino acid release was inversely correlated to the concentration of KCl used. However, at 50 mM K+, one-third of the stimulated release remained which was external Ca2+-independent but insensitive to SKF 100330 A. This release was prevented by BAPTA, thapsigargin or dantrolene; it also was inhibited by blocking in mitochondria the ATP production with oligomycin, the H+-dependent Ca2+ uniporter with RU 360, the Na+/Ca2+ exchanger with CGP 37157 or by lowering extraterminal [Na+]. In fluorescence experiments with fura-2/AM, 50 mM K+ (in Ca2+ free medium) caused elevation of cytosolic [Ca2+] that was sensitive to thapsigargin or CGP 37157; these compounds produced partially additive effects. When exocytosis was monitored with the fluorescent dye acridine orange, the fluorescence elicited by 50 mM K+ was sensitive to thapsigargin or CGP 37157, which produced additive effects, and to low-Na+ media. To conclude, extracellular K+ concentrations occurring in the CNS in certain pathological conditions provoke GABA release by mechanisms different from classical exocytosis. These include carrier-mediated release and internal Ca2+-dependent exocytosis; in the latter, mitochondrial Ca2+ seems to play a primary role. | lld:pubmed |
| pubmed-article:11841577 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11841577 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11841577 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11841577 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11841577 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:11841577 | pubmed:issn | 0022-3042 | lld:pubmed |
| pubmed-article:11841577 | pubmed:author | pubmed-author:RaiteriLucaL | lld:pubmed |
| pubmed-article:11841577 | pubmed:author | pubmed-author:StiglianiSara... | lld:pubmed |
| pubmed-article:11841577 | pubmed:author | pubmed-author:ZeddaLucaL | lld:pubmed |
| pubmed-article:11841577 | pubmed:author | pubmed-author:RaiteriMauriz... | lld:pubmed |
| pubmed-article:11841577 | pubmed:author | pubmed-author:BonannoGiamba... | lld:pubmed |
| pubmed-article:11841577 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11841577 | pubmed:volume | 80 | lld:pubmed |
| pubmed-article:11841577 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11841577 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11841577 | pubmed:pagination | 706-14 | lld:pubmed |
| pubmed-article:11841577 | pubmed:dateRevised | 2006-11-20 | lld:pubmed |
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| pubmed-article:11841577 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11841577 | pubmed:articleTitle | Multiple mechanisms of transmitter release evoked by "pathologically" elevated extracellular [K+]: involvement of transporter reversal and mitochondrial calcium. | lld:pubmed |
| pubmed-article:11841577 | pubmed:affiliation | Department of Experimental Medicine, Pharmacology and Toxicology Section, University of Genova, Genova, Italy. | lld:pubmed |
| pubmed-article:11841577 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11841577 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:11841577 | lld:pubmed |
