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Temporal Characteristics of Potassium‐Stimulated Acetylcholine Release and Inactivation of Calcium Influx in Rat Brain Synaptosomes
Author(s) -
Suszkiw J. B.,
O'Leary M. E.
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.tb04820.x
Subject(s) - depolarization , biophysics , chemistry , acetylcholine , calcium , stimulation , potassium , synaptosome , endocrinology , biology , organic chemistry
The time course of Ca 2+ ‐dependent [ 3 H]acetylcholine ([ 3 H]ACh) release and inactivation of 45 Ca 2+ entry were examined in rat brain synaptosomes depolarized by 45 m M [K + ] o . Under conditions where the intrasynaptosomal stores of releasable [ 3 H]ACh were neither exhausted nor replenished in the course of stimulation, the K + ‐evoked release consisted of a major (40% of the releasable [ 3 H]ACh pool), rapidly terminating phase ( t 1/2 = 17.8 s), and a subsequent, slow efflux that could be detected only during a prolonged, maintained depolarization. The time course of inactivation of K + ‐stimulated Ca 2+ entry suggests the presence of fast‐inactivating, slow‐inactivating, and noninactivating, or very slowly inactivating, components. The fast‐inactivating component of the K + ‐stimulated Ca 2+ entry into synaptosomes appears to be responsible for the rapidly terminating phase of transmitter release during the first 60 s of K + stimulus. The noninactivating Ca 2+ entry may account for the slow phase of transmitter release. These results indicate that under conditions of maintained depolarization of synaptosomes by high [K + ] o the time course and the amount of transmitter released may be a function of the kinetics of inactivation of the voltage‐dependent Ca channels.