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Characterization of Nicotinic Receptor‐Mediated [ 3 H]Dopamine Release from Synaptosomes Prepared from Mouse Striatum
Author(s) -
Grady Sharon,
Marks Michael J.,
Wonnacott Susan,
Collins Allan C.
Publication year - 1992
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.1471-4159.1992.tb08322.x
Subject(s) - mecamylamine , nicotinic agonist , dopamine , nicotine , chemistry , striatum , nicotinic antagonist , potency , pharmacology , alpha 4 beta 2 nicotinic receptor , synaptosome , receptor , nicotinic acetylcholine receptor , endocrinology , biology , biochemistry , neuroscience , in vitro
This study establishes that presynaptic nicotinic receptors modulate dopamine release in the mouse striatum. Nicotinic agonists elicit a dose‐dependent increase in the release of [ 3 H]dopamine from synaptosomes prepared from mouse striatum. At low concentrations, this release is Ca 2+ dependent, whereas at higher concentrations Ca 2+ ‐independent, mecamylamine‐insensitive release was also observed. The Ca 2+ ‐dependent nicotine‐evoked release was not blocked by α‐bungarotoxin but was effectively blocked by neuronal bungarotoxin as well as several other nicotinic receptor antagonists. The relationship between potency for stimulation of release for agonists and potency for inhibition of release for antagonists was compared to the affinity of these compounds for the [ 3 H]nicotine binding site. The overall correlation between release and binding potency was not high, but the drugs may be classified into separate groups, each of which has a high correlation with binding. This finding suggests either that more than one nicotinic receptor regulates dopamine release or that not all agonists interact with the same receptor in an identical fashion.