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Inhibition by Quinacrine of Depolarization‐Induced Acetylcholine Release and Calcium Influx in Rat Brain Cortical Synaptosomes
Author(s) -
Baba Akemichi,
Ohta Akira,
Iwata Heitaroh
Publication year - 1983
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1983.tb08152.x
Subject(s) - depolarization , acetylcholine , calcium , chemistry , synaptosome , biophysics , neuroscience , endocrinology , biology , organic chemistry
The effects of quinacrine on depolarization‐induced [ 3 H]acetylcholine (ACh) release and 45 Ca 2+ influx were examined in rat brain cortical synaptosomes. Quinacrine significantly reduced the stimulated release of [ 3 H]ACh by high K + and veratridine without affecting the spontaneous efflux from the preloaded synaptosomes. Quinacrine had no effect on ionophore A23187‐induced release of [ 3 H]ACh from the synaptosomes. Quinacrine (100 μ M ) markedly diminished the stimulated Ca 2+ influx by veratridine and high K + but not that by “Na + ‐free.” Trifluoperazine, a potent calmodulin antagonist, inhibited both Ca 2+ influx and ACh release induced by the depolarizing agents. Inhibitory potencies of the two drugs on ACh release and Ca 2+ influx were compared with the antagonism of calmodulin by two drugs, suggesting that the inhibition of depolarization‐induced Ca 2+ influx and ACh release by these drugs could not be explained by the antagonism of calmodulin.