pubmed-article:17181555 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C0085262 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C0034830 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C0006685 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C1948027 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
pubmed-article:17181555 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
pubmed-article:17181555 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:17181555 | pubmed:dateCreated | 2007-2-1 | lld:pubmed |
pubmed-article:17181555 | pubmed:abstractText | Neuronal nicotinic acetylcholine receptors (nAChRs) are ligand-gated cation channels that can modulate various neuronal processes by altering intracellular Ca(2+) levels. Following nAChR stimulation Ca(2+) can enter cells either directly, through the intrinsic ion channel, or indirectly following voltage-operated Ca(2+) channel (VOCC) activation; Ca(2+) levels can subsequently be amplified via Ca(2+)-induced Ca(2+) release from intracellular stores. We have used subtype-selective nAChR agonists to investigate the Ca(2+) sources contributing to alpha7 and non-alpha7 nAChR-mediated increases in intracellular Ca(2+) in PC12 cells. Application of the alpha7 nAChR positive allosteric modulator PNU 120596 (10 mum), in conjunction with the alpha7 nAChR agonist, compound A [(R)-N-(1-azabicyclo[2.2.2]oct-3-yl)(5-(2-pyridyl)thiophene-2-carboxamide), 10 nm], produces a rapid increase in fluo-3 fluorescence that is prevented by the selective alpha7 nAChR antagonist alpha-bungarotoxin. The non-alpha7 nAChR agonist 5-Iodo-A-85380 produces alpha-bungarotoxin-insensitive increases in intracellular Ca(2+) (EC(50) = 11.2 mum). Using these selective agonists or KCl in conjunction with general and selective VOCC inhibitors, we demonstrate that the primary route of Ca(2+) entry following either non-alpha7 nAChR activation or KCl stimulation is via L-type VOCCs. In contrast, the alpha7 nAChR-mediated response is unaffected by VOCC blockers but is inhibited by modulators of intracellular Ca(2+) stores. These results indicate that alpha7 and non-alpha7 nAChRs are differentially coupled to Ca(2+)-induced Ca(2+) release and VOCCs, respectively. | lld:pubmed |
pubmed-article:17181555 | pubmed:language | eng | lld:pubmed |
pubmed-article:17181555 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17181555 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17181555 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17181555 | pubmed:month | Feb | lld:pubmed |
pubmed-article:17181555 | pubmed:issn | 0022-3042 | lld:pubmed |
pubmed-article:17181555 | pubmed:author | pubmed-author:WonnacottSusa... | lld:pubmed |
pubmed-article:17181555 | pubmed:author | pubmed-author:KewJames N... | lld:pubmed |
pubmed-article:17181555 | pubmed:author | pubmed-author:MokM H... | lld:pubmed |
pubmed-article:17181555 | pubmed:author | pubmed-author:DickinsonJane... | lld:pubmed |
pubmed-article:17181555 | pubmed:author | pubmed-author:HanrottKathar... | lld:pubmed |
pubmed-article:17181555 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17181555 | pubmed:volume | 100 | lld:pubmed |
pubmed-article:17181555 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17181555 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17181555 | pubmed:pagination | 1089-96 | lld:pubmed |
pubmed-article:17181555 | pubmed:dateRevised | 2010-6-4 | lld:pubmed |
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pubmed-article:17181555 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17181555 | pubmed:articleTitle | Differential coupling of alpha7 and non-alpha7 nicotinic acetylcholine receptors to calcium-induced calcium release and voltage-operated calcium channels in PC12 cells. | lld:pubmed |
pubmed-article:17181555 | pubmed:affiliation | Department of Biology & Biochemistry, University of Bath, Bath, UK. | lld:pubmed |
pubmed-article:17181555 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17181555 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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