| pubmed-article:6131420 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:6131420 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:6131420 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:6131420 | lifeskim:mentions | umls-concept:C0006685 | lld:lifeskim |
| pubmed-article:6131420 | lifeskim:mentions | umls-concept:C1550548 | lld:lifeskim |
| pubmed-article:6131420 | lifeskim:mentions | umls-concept:C1555714 | lld:lifeskim |
| pubmed-article:6131420 | lifeskim:mentions | umls-concept:C1705654 | lld:lifeskim |
| pubmed-article:6131420 | pubmed:issue | 1206 | lld:pubmed |
| pubmed-article:6131420 | pubmed:dateCreated | 1983-4-15 | lld:pubmed |
| pubmed-article:6131420 | pubmed:abstractText | We describe a model for the mechanism by which Ca channel inactivation might depend on calcium entry. Ca is assumed to bind to a site at the internal membrane surface to cause inactivation of Ca channels. We assume that Ca that enters through the membrane accumulates in a submembrane compartment and also make simplifying assumptions about Ca buffering and removal. Our model predicts the results of single- and double-pulse voltage-clamp experiments well. The predicted turn-off of Ca current is non-exponential. The model also predicts that procedures that slow inactivation will increase peak Ca current and suggests that both two-phase turn-off of currents and failure of normalized current to recover to 1.0 in two-pulse experiments may be explained without assuming a voltage-dependent component of inactivation or two populations of Ca channels. | lld:pubmed |
| pubmed-article:6131420 | pubmed:language | eng | lld:pubmed |
| pubmed-article:6131420 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6131420 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:6131420 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:6131420 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:6131420 | pubmed:issn | 0080-4649 | lld:pubmed |
| pubmed-article:6131420 | pubmed:author | pubmed-author:StanfieldP... | lld:pubmed |
| pubmed-article:6131420 | pubmed:author | pubmed-author:StandenN BNB | lld:pubmed |
| pubmed-article:6131420 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:6131420 | pubmed:day | 22 | lld:pubmed |
| pubmed-article:6131420 | pubmed:volume | 217 | lld:pubmed |
| pubmed-article:6131420 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:6131420 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:6131420 | pubmed:pagination | 101-10 | lld:pubmed |
| pubmed-article:6131420 | pubmed:dateRevised | 2007-4-30 | lld:pubmed |
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| pubmed-article:6131420 | pubmed:meshHeading | pubmed-meshheading:6131420-... | lld:pubmed |
| pubmed-article:6131420 | pubmed:year | 1982 | lld:pubmed |
| pubmed-article:6131420 | pubmed:articleTitle | A binding-site model for calcium channel inactivation that depends on calcium entry. | lld:pubmed |
| pubmed-article:6131420 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:6131420 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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