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Presynaptic release probability and readily releasable pool size are regulated by two independent mechanisms during posttetanic potentiation at the calyx of Held synapse

Cited 49 time in Web of Science Cited 52 time in Scopus
Authors
Lee, Jae Sung; Kim, Myoung-Hwan; Ho, Won-Kyung; Lee, Suk-Ho
Issue Date
2008-08-08
Publisher
Society for Neuroscience
Citation
J Neurosci. 28(32):7945-7953
Keywords
AnimalsBrain Stem/drug effects/metabolism/*physiologyCalcium/*metabolismCalcium Channel Blockers/pharmacologyElectric StimulationEnzyme Activation/physiologyExcitatory Postsynaptic PotentialsMitochondria/metabolismMyosin-Light-Chain Kinase/antagonists & inhibitors/*metabolismOnium Compounds/pharmacologyOrganophosphorus Compounds/pharmacologyPatch-Clamp TechniquesPresynaptic Terminals/drug effects/metabolism/*physiologyProbabilityProtein Kinase C/metabolismProtein Kinase Inhibitors/pharmacologyRatsRats, Sprague-DawleyRuthenium Compounds/pharmacologySodium/metabolism
Abstract
At the immature calyx of Held, the fast decay phase of a Ca(2+) transient induced by tetanic stimulation (TS) was followed by a period of elevated [Ca(2+)](i) for tens of seconds, referred to as posttetanic residual calcium (Ca(res)). We investigated the source of Ca(res) and its contribution to posttetanic potentiation (PTP). After TS (100 Hz for 4 s), posttetanic Ca(res) at the calyx of Held was largely abolished by tetraphenylphosphonium (TPP(+)) or Ru360, which inhibit mitochondrial Na(+)-dependent Ca(2+) efflux and Ca(2+) uniporter, respectively. Whereas the control PTP lasted longer than Ca(res), inhibition of Ca(res) by TPP(+) resulted in preferential suppression of the early phase of PTP, the decay time course of which well matched with that of Ca(res). TS induced significant increases in release probability (P(r)) and the size of the readily releasable pool (RRP), which were estimated from plots of cumulative EPSC amplitudes. TPP(+) or Ru360 suppressed the posttetanic increase in P(r), whereas it had little effect on the increase in RRP size. Moreover, the posttetanic increase in P(r), but not in RRP size, showed a linear correlation with the amount of Ca(res). In contrast, myosin light chain kinase (MLCK) inhibitors and blebbistatin reduced the posttetanic increase in RRP size with no effect on the increase in P(r). Application of TPP(+) in the presence of MLCK inhibitor peptide caused further suppression of PTP. These findings suggest that Ca(res) released from mitochondria and activation of MLCK are primarily responsible for the increase in P(r) and that in the RRP size, respectively.
ISSN
1529-2401 (Electronic)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18685020

http://www.jneurosci.org/cgi/reprint/28/32/7945.pdf

http://hdl.handle.net/10371/68161
DOI
https://doi.org/10.1523/JNEUROSCI.2165-08.2008
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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