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Effects of intravesicular loading of a Ca 2+ chelator and depolymerization of actin fibers on neurotransmitter release in frog motor nerve terminals
Author(s) -
Narita Kazuhiko,
Suzuki Naoya,
Himi Naoyuki,
Murayama Takashi,
Nakagawa Toshitaka,
Okabe Naohiko,
NakamuraMaruyama Emi,
Hayashi Norito,
Sakamoto Issei,
Miyamoto Osamu,
Kuba Kenji
Publication year - 2019
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.14353
Subject(s) - synaptic vesicle , egta , neurotransmitter , chemistry , biophysics , tetanic stimulation , neurotransmission , ryanodine receptor , vesicle , stimulation , excitatory postsynaptic potential , intracellular , neuroscience , calcium , biochemistry , biology , receptor , membrane , organic chemistry
Ca 2+ ‐induced Ca 2+ release ( CICR ) via type‐3 ryanodine receptor enhances neurotransmitter release in frog motor nerve terminals. To test a possible role of synaptic vesicle in CICR , we examined the effects of loading of EGTA , a Ca 2+ chelator, into synaptic vesicles and depolymerization of actin fibers. Intravesicular EGTA loading via endocytosis inhibited the ryanodine sensitive enhancement of transmitter release induced by tetanic stimulation and the associated rises in intracellular‐free Ca 2+ ([Ca 2+ ] i : Ca 2+ transients). Latrunculin A, a depolymerizer of actin fibers, enhanced both spontaneous and stimulation‐induced transmitter release, but inhibited the enhancement of transmitter release elicited by successive tetanic stimulation. The results suggest a possibility that the activation of CICR from mobilized synaptic vesicles caused the enhancement of neurotransmitter release.