Linked Life Data

10736317

Source:http://linkedlifedata.com/resource/pubmed/id/10736317

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2000-5-10
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.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-10197523, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-10479687, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-1148488, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-1350109, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-13673292, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-1432708, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-1484356, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-14898516, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-165285, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-174144, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-2317553, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-2412607, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-2501716, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-4205467, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-4296699, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-4366843, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-6128372, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-6128373, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-6767024, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-7512352, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-7612860, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-7718232, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-7760519, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-7931551, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-7935764, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-7935792, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-8229800, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-8301352, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-8874493, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-8982154, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9003548, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9003551, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9017193, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9115741, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9234194, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9350620, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9457637, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9512051, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9518701, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9806968, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9874372, http://linkedlifedata.com/resource/pubmed/commentcorrection/10736317-9874373
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1295
pubmed:author
pubmed:issnType
Print
pubmed:volume
115
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
519-32
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Functional coupling of Ca(2+) channels to ryanodine receptors at presynaptic terminals. Amplification of exocytosis and plasticity.
pubmed:affiliation
Department of Physiology, Kawasaki Medical School, Kurashiki 701-0192, Japan.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't