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| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0001041 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0021549 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
| pubmed-article:15342646 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
| pubmed-article:15342646 | pubmed:issue | 47 | lld:pubmed |
| pubmed-article:15342646 | pubmed:dateCreated | 2004-11-15 | lld:pubmed |
| pubmed-article:15342646 | pubmed:abstractText | Intracellular Ca2+ store release contributes to activity-dependent synaptic plasticity in the central nervous system by modulating the amplitude, propagation, and temporal dynamics of cytoplasmic Ca2+ changes. However, neuronal Ca2+ stores can be relatively insensitive to increases in the store-mobilizing messenger inositol 1,4,5-trisphosphate (IP3). Using a fluorescent biosensor we have visualized M1 muscarinic acetylcholine (mACh) receptor signaling in individual hippocampal neurons and observed increased IP3 production in the absence of concurrent Ca2+ store release. However, coincident glutamate-mediated synaptic activity elicited enhanced and oscillatory IP3 production that was dependent upon ongoing mACh receptor stimulation and S-alpha-amino-3-hydroxy-5-methyl-4-isoazolepropionic acid receptor activation of Ca2+ entry. Moreover, the enhanced levels of IP3 now mobilized Ca2+ from intracellular stores that were refractory to the activation of mACh receptors alone. We conclude that convergent ionotropic and metabotropic receptor inputs can facilitate Ca2+ signaling by enhancing IP3 production as well as augmenting release by Ca2+-induced Ca2+ release. | lld:pubmed |
| pubmed-article:15342646 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15342646 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15342646 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15342646 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15342646 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15342646 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15342646 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:15342646 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:15342646 | pubmed:author | pubmed-author:John... | lld:pubmed |
| pubmed-article:15342646 | pubmed:author | pubmed-author:NashMark SMS | lld:pubmed |
| pubmed-article:15342646 | pubmed:author | pubmed-author:WilletsJonath... | lld:pubmed |
| pubmed-article:15342646 | pubmed:author | pubmed-author:NahorskiStefa... | lld:pubmed |
| pubmed-article:15342646 | pubmed:author | pubmed-author:BillupsBrianB | lld:pubmed |
| pubmed-article:15342646 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15342646 | pubmed:day | 19 | lld:pubmed |
| pubmed-article:15342646 | pubmed:volume | 279 | lld:pubmed |
| pubmed-article:15342646 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15342646 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15342646 | pubmed:pagination | 49036-44 | lld:pubmed |
| pubmed-article:15342646 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:15342646 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15342646 | pubmed:articleTitle | Synaptic activity augments muscarinic acetylcholine receptor-stimulated inositol 1,4,5-trisphosphate production to facilitate Ca2+ release in hippocampal neurons. | lld:pubmed |
| pubmed-article:15342646 | pubmed:affiliation | Department of Cell Physiology & Pharmacology, University of Leicester, Maurice Shock Medical Sciences Building, University Road, Leicester, LE1 9HN, United Kingdom. | lld:pubmed |
| pubmed-article:15342646 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15342646 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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