pubmed-article:12065669 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C0034830 | lld:lifeskim |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C1698986 | lld:lifeskim |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:12065669 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
pubmed-article:12065669 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:12065669 | pubmed:dateCreated | 2002-6-14 | lld:pubmed |
pubmed-article:12065669 | pubmed:abstractText | Neuronal nicotinic acetylcholine receptors (nAChR) can regulate several neuronal processes through Ca2+-dependent mechanisms. The versatility of nAChR-mediated responses presumably reflects the spatial and temporal characteristics of local changes in intracellular Ca2+ arising from a variety of sources. The aim of this study was to analyse the components of nicotine-evoked Ca2+ signals in SH-SY5Y cells, by monitoring fluorescence changes in cells loaded with fluo-3 AM. Nicotine (30 microm) generated a rapid elevation in cytoplasmic Ca2+ that was partially and additively inhibited (40%) by alpha7 and alpha3beta2* nAChR subtype selective antagonists; alpha3beta4* nAChR probably account for the remaining response (60%). A substantial blockade (80%) by CdCl2 (100 microm) indicates that voltage-operated Ca2+ channels (VOCC) mediate most of the nicotine-evoked response, although the alpha7 selective antagonist alpha-bungarotoxin (40 nm) further decreased the CdCl2- resistant component. The elevation of intracellular Ca2+ levels provoked by nicotine was sustained for at least 10 min and required the persistent activation of nAChR throughout the response. Intracellular Ca2+ stores were implicated in both the initial and sustained nicotine-evoked Ca2+ responses, by the blockade observed after ryanodine (30 microm) and the inositoltriphosphate (IP3)-receptor antagonist, xestospongin-c (10 microm). Thus, nAChR subtypes are differentially coupled to specific sources of Ca2+: activation of nAChR induces a sustained elevation of intracellular Ca2+ levels which is highly dependent on the activation of VOCC, and also involves Ca2+ release from ryanodine and IP3-dependent intracellular stores. Moreover, the alpha7, but not alpha3beta2* nAChR, are responsible for a fraction of the VOCC-independent nicotine-evoked Ca2+ increase that appears to be functionally coupled to ryanodine sensitive Ca2+ stores. | lld:pubmed |
pubmed-article:12065669 | pubmed:language | eng | lld:pubmed |
pubmed-article:12065669 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12065669 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12065669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12065669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:12065669 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12065669 | pubmed:month | May | lld:pubmed |
pubmed-article:12065669 | pubmed:issn | 0022-3042 | lld:pubmed |
pubmed-article:12065669 | pubmed:author | pubmed-author:WonnacottSusa... | lld:pubmed |
pubmed-article:12065669 | pubmed:author | pubmed-author:Dajas-Bailado... | lld:pubmed |
pubmed-article:12065669 | pubmed:author | pubmed-author:MoggAdrian... | lld:pubmed |
pubmed-article:12065669 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12065669 | pubmed:volume | 81 | lld:pubmed |
pubmed-article:12065669 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12065669 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12065669 | pubmed:pagination | 606-14 | lld:pubmed |
pubmed-article:12065669 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:12065669 | pubmed:meshHeading | pubmed-meshheading:12065669... | lld:pubmed |
pubmed-article:12065669 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12065669 | pubmed:articleTitle | Intracellular Ca2+ signals evoked by stimulation of nicotinic acetylcholine receptors in SH-SY5Y cells: contribution of voltage-operated Ca2+ channels and Ca2+ stores. | lld:pubmed |
pubmed-article:12065669 | pubmed:affiliation | Department of Biology and Biochemistry, University of Bath, Bath, UK. | lld:pubmed |
pubmed-article:12065669 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12065669 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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