| pubmed-article:10736317 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10736317 | lifeskim:mentions | umls-concept:C0206181 | lld:lifeskim |
| pubmed-article:10736317 | lifeskim:mentions | umls-concept:C0015283 | lld:lifeskim |
| pubmed-article:10736317 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
| pubmed-article:10736317 | lifeskim:mentions | umls-concept:C0917729 | lld:lifeskim |
| pubmed-article:10736317 | lifeskim:mentions | umls-concept:C0678558 | lld:lifeskim |
| pubmed-article:10736317 | lifeskim:mentions | umls-concept:C1948027 | lld:lifeskim |
| pubmed-article:10736317 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:10736317 | lifeskim:mentions | umls-concept:C1521871 | lld:lifeskim |
| pubmed-article:10736317 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:10736317 | pubmed:dateCreated | 2000-5-10 | lld:pubmed |
| pubmed-article:10736317 | pubmed:abstractText | Ca(2+)-induced Ca(2+) release (CICR) enhances a variety of cellular Ca(2+) signaling and functions. How CICR affects impulse-evoked transmitter release is unknown. At frog motor nerve terminals, repetitive Ca(2+) entries slowly prime and subsequently activate the mechanism of CICR via ryanodine receptors and asynchronous exocytosis of transmitters. Further Ca(2+) entry inactivates the CICR mechanism and the absence of Ca(2+) entry for >1 min results in its slow depriming. We now report here that the activation of this unique CICR markedly enhances impulse-evoked exocytosis of transmitter. The conditioning nerve stimulation (10-20 Hz, 2-10 min) that primes the CICR mechanism produced the marked enhancement of the amplitude and quantal content of end-plate potentials (EPPs) that decayed double exponentially with time constants of 1.85 and 10 min. The enhancement was blocked by inhibitors of ryanodine receptors and was accompanied by a slight prolongation of the peak times of EPP and the end-plate currents estimated from deconvolution of EPP. The conditioning nerve stimulation also enhanced single impulse- and tetanus-induced rises in intracellular Ca(2+) in the terminals with little change in time course. There was no change in the rate of growth of the amplitudes of EPPs in a short train after the conditioning stimulation. On the other hand, the augmentation and potentiation of EPP were enhanced, and then decreased in parallel with changes in intraterminal Ca(2+) during repetition of tetani. The results suggest that ryanodine receptors exist close to voltage-gated Ca(2+) channels in the presynaptic terminals and amplify the impulse-evoked exocytosis and its plasticity via CICR after Ca(2+)-dependent priming. | lld:pubmed |
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| pubmed-article:10736317 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10736317 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10736317 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10736317 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10736317 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10736317 | pubmed:issn | 0022-1295 | lld:pubmed |
| pubmed-article:10736317 | pubmed:author | pubmed-author:NaritaKK | lld:pubmed |
| pubmed-article:10736317 | pubmed:author | pubmed-author:KubaKK | lld:pubmed |
| pubmed-article:10736317 | pubmed:author | pubmed-author:HuangSS | lld:pubmed |
| pubmed-article:10736317 | pubmed:author | pubmed-author:OchiKK | lld:pubmed |
| pubmed-article:10736317 | pubmed:author | pubmed-author:AkitaTT | lld:pubmed |
| pubmed-article:10736317 | pubmed:author | pubmed-author:HachisukaJJ | lld:pubmed |
| pubmed-article:10736317 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10736317 | pubmed:volume | 115 | lld:pubmed |
| pubmed-article:10736317 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10736317 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10736317 | pubmed:pagination | 519-32 | lld:pubmed |
| pubmed-article:10736317 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10736317 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10736317 | pubmed:articleTitle | Functional coupling of Ca(2+) channels to ryanodine receptors at presynaptic terminals. Amplification of exocytosis and plasticity. | lld:pubmed |
| pubmed-article:10736317 | pubmed:affiliation | Department of Physiology, Kawasaki Medical School, Kurashiki 701-0192, Japan. | lld:pubmed |
| pubmed-article:10736317 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10736317 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:10736317 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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