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Acetylcholine Releases ATP from Varicosities Isolated from Guinea Pig Myenteric Plexus
Author(s) -
White Thomas D.,
AlHumayyd Mohammed
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.tb08094.x
Subject(s) - veratridine , acetylcholine , bethanechol , hexamethonium , tetrodotoxin , myenteric plexus , muscarinic acetylcholine receptor , cholinergic , nicotinic agonist , chemistry , endocrinology , medicine , depolarization , biology , biochemistry , receptor , sodium , sodium channel , organic chemistry , immunohistochemistry
The effects of cholinergic agonists and antagonists on the release of ATP from isolated myenteric varicosities were studied using a firefly luciferin‐luciferase technique. In a previous study, acetylcholine and nicotine released ATP from isolated myenteric varicosities, whereas the muscarinic agonist bethanechol did not. In the present study, release of ATP by acetylcholine was shown to be Ca 2+ dependent. d ‐Tubocurarine competitively antagonized the release of ATP by either acetylcholine or nicotine. Maximal release of ATP by acetylcholine (10 ‐3 M ) was approximately 24% that observed with the depolarizing drug veratridine (5 x 10 5 M ), suggesting either that not all of the varicosities capable of releasing ATP possess nicotinic receptors or that acetyl‐choline does not depolarize the varicosities to the degree that veratridine does. Tetrodotoxin slightly but significantly reduced ATP release induced by acetylcholine or nicotine, indicating some involvement of Na + channels in the release process. Finally, 6‐hydroxydopamine pre‐treatment produced a 48% reduction in the acetylcholine‐evoked release of ATP, suggesting that much, but possibly not all, of the ATP release occurs from noradrenergic varicosities present in the preparation.