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Nicotinic Stimulation of [ 3 H]Acetylcholine Release from Mouse Cerebral Cortical Synaptosomes
Author(s) -
Rowell Peter P.,
Winkler Donald L.
Publication year - 1984
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.1471-4159.1984.tb06083.x
Subject(s) - hexamethonium , acetylcholine , nicotine , chemistry , nicotinic agonist , cholinergic , stimulation , depolarization , endocrinology , acetylcholine receptor , medicine , synaptosome , choline , nicotinic acetylcholine receptor , cholinesterase , biochemistry , receptor , biology , in vitro
The effects of nicotine and 1,1‐dimethyl‐4‐phenylpiperazinium (DMPP) on the release of newly synthesized [ 3 H]acetylcholine in mouse cerebral cortical synaptosomes were examined. Nicotine and DMPP produced increases in [ 3 H]acetylcholine release, over the level of spontaneous release, of 24% and 30%, respectively, of a maximum depolarization‐induced release produced by 50 m M potassium. The maximum effect was achieved at a concentration of 1 × 10 ‐4 M for both agents. The time course of release indicated a slow onset of action, reaching a maximum effect at 15 min of incubation. Both nicotine and DMPP also produced a slightly greater release of total tritium, measured in the absence of cholinesterase inhibition, than of [ 3 H]acetylcholine. The release induced by nicotine was completely antagonized by hexamethonium and was largely (58%) calciumdependent. Nicotine also produced an increase in [ 3 H]choline accumulation into synaptosomes. These results indicate that the nicotinic agonists nicotine and DMPP can produce a moderate enhancement of acetylcholine release by a receptor‐mediated action on cholinergic nerve terminals in the central nervous system.