pubmed-article:7931551 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7931551 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
pubmed-article:7931551 | lifeskim:mentions | umls-concept:C0242485 | lld:lifeskim |
pubmed-article:7931551 | lifeskim:mentions | umls-concept:C1609982 | lld:lifeskim |
pubmed-article:7931551 | lifeskim:mentions | umls-concept:C0439857 | lld:lifeskim |
pubmed-article:7931551 | lifeskim:mentions | umls-concept:C0392762 | lld:lifeskim |
pubmed-article:7931551 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:7931551 | lifeskim:mentions | umls-concept:C1627358 | lld:lifeskim |
pubmed-article:7931551 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:7931551 | pubmed:dateCreated | 1994-11-14 | lld:pubmed |
pubmed-article:7931551 | pubmed:abstractText | We simultaneously measured presynaptic free calcium ion concentration ([Ca2+]i) and synaptic strength at the crayfish claw opener neuromuscular junction (nmj) under a variety of experimental conditions. Our experiments were designed both to test the hypothesis that elevated [Ca2+]i is necessary and sufficient for the induction of a form of synaptic enhancement that persists for several seconds after tetanic stimulation--augmentation--and to determine the quantitative relationship between elevated [Ca2+]i and this enhancement. Action potential trains increased [Ca2+]i and enhanced transmission. During the decay phase of synaptic enhancement known as augmentation (time constant of decay approximately 7 sec at 20 degrees C with < 200 microM fura-2 in terminals), [Ca2+]i was elevated 700 nM or less above rest and an essentially linear relationship between [Ca2+]i and enhancement was observed. Introduction of exogenous Ca2+ buffers into the presynaptic terminal slowed the buildup and recovery kinetics of both [Ca2+]i and the component of synaptic enhancement corresponding to augmentation. The slope of the relationship relating delta [Ca2+]i to augmentation was not changed. The time course of augmentation and recovery of [Ca2+]i remained correlated as the temperature of the preparation was changed from about 10 degrees C to 20 degrees C, but the quantitative relationship of enhancement to [Ca2+]i was increased more than two- to threefold. During moderate frequency trains of action potentials, a slowly developing component of the total synaptic enhancement was approximately linearly related to residual [Ca2+]i measured with fura-2. The quantitative relationship between [Ca2+]i and this component of synaptic enhancement during trains was the same as that during synaptic augmentation after trains.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
pubmed-article:7931551 | pubmed:language | eng | lld:pubmed |
pubmed-article:7931551 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7931551 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:7931551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:7931551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7931551 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7931551 | pubmed:month | Oct | lld:pubmed |
pubmed-article:7931551 | pubmed:issn | 0270-6474 | lld:pubmed |
pubmed-article:7931551 | pubmed:author | pubmed-author:DelaneyK RKR | lld:pubmed |
pubmed-article:7931551 | pubmed:author | pubmed-author:READB EBE | lld:pubmed |
pubmed-article:7931551 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7931551 | pubmed:volume | 14 | lld:pubmed |
pubmed-article:7931551 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7931551 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7931551 | pubmed:pagination | 5885-902 | lld:pubmed |
pubmed-article:7931551 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:7931551 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:7931551 | pubmed:articleTitle | A quantitative measurement of the dependence of short-term synaptic enhancement on presynaptic residual calcium. | lld:pubmed |
pubmed-article:7931551 | pubmed:affiliation | Biological Computation Research Department, AT&T Bell Laboratories, Murray Hill, New Jersey 07974. | lld:pubmed |
pubmed-article:7931551 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7931551 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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