pubmed-article:1370370 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1370370 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
pubmed-article:1370370 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
pubmed-article:1370370 | lifeskim:mentions | umls-concept:C0034830 | lld:lifeskim |
pubmed-article:1370370 | lifeskim:mentions | umls-concept:C0031164 | lld:lifeskim |
pubmed-article:1370370 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
pubmed-article:1370370 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:1370370 | pubmed:dateCreated | 1992-2-20 | lld:pubmed |
pubmed-article:1370370 | pubmed:abstractText | Two properties were found to distinguish neuronal from muscle nicotinic acetylcholine receptors (nAChRs). First, neuronal nAChRs have a greater Ca2+ permeability. The high Ca2+ flux through neuronal nAChRs activates a Ca(2+)-dependent Cl- conductance, and the Ca2+ to Cs+ permeability ratio (PCa/PCs) is 7 times greater for neuronal than for muscle nAChRs. A second difference between the receptor types is that neuronal nAChRs are potently modulated by physiological levels of external Ca2+. Neuronal nAChR currents are enhanced by external Ca2+ in a dose-dependent manner. The results indicate that changes in extracellular Ca2+ modulate neuronal nAChRs and may modulate cholinergic synapses in the CNS. Also, activation of neuronal nAChRs produces a significant influx of Ca2+ that could be an important intracellular signal. | lld:pubmed |
pubmed-article:1370370 | pubmed:language | eng | lld:pubmed |
pubmed-article:1370370 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1370370 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1370370 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1370370 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1370370 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1370370 | pubmed:month | Jan | lld:pubmed |
pubmed-article:1370370 | pubmed:issn | 0896-6273 | lld:pubmed |
pubmed-article:1370370 | pubmed:author | pubmed-author:PatrickJJ | lld:pubmed |
pubmed-article:1370370 | pubmed:author | pubmed-author:AmadorMM | lld:pubmed |
pubmed-article:1370370 | pubmed:author | pubmed-author:DaniJ AJA | lld:pubmed |
pubmed-article:1370370 | pubmed:author | pubmed-author:LuetjeC WCW | lld:pubmed |
pubmed-article:1370370 | pubmed:author | pubmed-author:VerninoSS | lld:pubmed |
pubmed-article:1370370 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1370370 | pubmed:volume | 8 | lld:pubmed |
pubmed-article:1370370 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1370370 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1370370 | pubmed:pagination | 127-34 | lld:pubmed |
pubmed-article:1370370 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:1370370 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1370370 | pubmed:articleTitle | Calcium modulation and high calcium permeability of neuronal nicotinic acetylcholine receptors. | lld:pubmed |
pubmed-article:1370370 | pubmed:affiliation | Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030-3498. | lld:pubmed |
pubmed-article:1370370 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1370370 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:1370370 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:1370370 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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