| pubmed-article:2206532 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2206532 | lifeskim:mentions | umls-concept:C1179435 | lld:lifeskim |
| pubmed-article:2206532 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:2206532 | lifeskim:mentions | umls-concept:C1705248 | lld:lifeskim |
| pubmed-article:2206532 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:2206532 | lifeskim:mentions | umls-concept:C1548799 | lld:lifeskim |
| pubmed-article:2206532 | lifeskim:mentions | umls-concept:C1524073 | lld:lifeskim |
| pubmed-article:2206532 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:2206532 | lifeskim:mentions | umls-concept:C0449432 | lld:lifeskim |
| pubmed-article:2206532 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:2206532 | pubmed:dateCreated | 1990-11-21 | lld:pubmed |
| pubmed-article:2206532 | pubmed:abstractText | High-threshold Ca2+ current triggers neurotransmitter release, but the existence, significance, and correct identification of different types of high-threshold Ca2+ channels remain controversial. We show selective inhibition of a rapidly inactivating component of high-threshold Ca2+ current in rat sensory neurons by bursts of brief pulses that mimic trains of action potentials and by prolonged depolarization just above the normal rest potential. In contrast, a slowly inactivating component decreases only when sufficient Ca2+ accumulates within the cell. Thus, there are physiologically important differences: whereas availability of the transient component depends on the value of the rest potential and the pattern of a prior stimulus, the sustained component seems to provide a baseline level of voltage-dependent Ca2+ entry that is lost only when intracellular Ca2+ rises. | lld:pubmed |
| pubmed-article:2206532 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2206532 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2206532 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2206532 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2206532 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2206532 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2206532 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2206532 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2206532 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2206532 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:2206532 | pubmed:issn | 0896-6273 | lld:pubmed |
| pubmed-article:2206532 | pubmed:author | pubmed-author:SchroederJ... | lld:pubmed |
| pubmed-article:2206532 | pubmed:author | pubmed-author:McCleskeyE... | lld:pubmed |
| pubmed-article:2206532 | pubmed:author | pubmed-author:FischbachP... | lld:pubmed |
| pubmed-article:2206532 | pubmed:author | pubmed-author:MalyZZ | lld:pubmed |
| pubmed-article:2206532 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2206532 | pubmed:volume | 5 | lld:pubmed |
| pubmed-article:2206532 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2206532 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2206532 | pubmed:pagination | 445-52 | lld:pubmed |
| pubmed-article:2206532 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:meshHeading | pubmed-meshheading:2206532-... | lld:pubmed |
| pubmed-article:2206532 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2206532 | pubmed:articleTitle | Two components of high-threshold Ca2+ current inactivate by different mechanisms. | lld:pubmed |
| pubmed-article:2206532 | pubmed:affiliation | Department of Cell Biology and Physiology, Washington University, St. Louis, Missouri 63110. | lld:pubmed |
| pubmed-article:2206532 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2206532 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2206532 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:2206532 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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