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Ca 2+ o ‐Independent Veratridine‐Evoked Acetylcholine Release from Striatal Slices Is Not Inhibited by Vesamicol (AH5183): Mobilization of Distinct Transmitter Pools
Author(s) -
AdamVizi Vera,
Deri Z.,
Vizi E. S.,
Sershen H.,
Lajtha A.
Publication year - 1991
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.1471-4159.1991.tb02561.x
Subject(s) - veratridine , acetylcholine , muscarine , chemistry , stimulation , cholinergic , synaptic vesicle , biophysics , muscarinic acetylcholine receptor , endocrinology , biology , biochemistry , vesicle , sodium , sodium channel , receptor , membrane , organic chemistry
The effect of 2‐(4‐phenylpiperidino)cyclohexanol (AH5183 or vesamicol), a compound known to block the uptake of acetylcholine (ACh) into cholinergic synaptic vesicles, on the release of endogenous and [ 14 C]ACh from slices of rat striatum was investigated. ACh release was evoked either by electrical stimulation or by veratridine. The effect of electrical stimulation was entirely dependent on external Ca 2+ . By contrast, veratridine (40 μ M ) also enhanced ACh release in the absence of Ca 2+ . Indeed, with veratridine two components were clearly distinguished: one dependent on external Ca 2+ and the other not. Vesamicol inhibited [ 14 C]ACh release evoked by both veratridine and electrical stimulation in the presence of external Ca 2+ , provided it was added to the tissue prior to loading with [ 14 C]choline. With the same treatment vesamicol only slightly affected the release of endogenous ACh. Under the same conditions the Ca 2+ ‐independent [ 14 C]ACh release evoked by veratridine was not prevented by vesamicol. The differential responsiveness to vesamicol suggests that ACh pools involved in Ca 2+ o ‐dependent ACh release are different from those mobilized during Ca 2+ o ‐independent ACh release.