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Differential inhibition of the release of endogenous and newly synthesized acetylcholine from Torpedo synaptosomes by presynaptic muscarinic receptors
Author(s) -
Luz S.,
Pinchasi I.,
Michaelson D.M.
Publication year - 1983
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(83)80007-6
Subject(s) - oxotremorine , muscarinic acetylcholine receptor , torpedo , acetylcholine , chemistry , muscarinic acetylcholine receptor m4 , muscarinic acetylcholine receptor m3 , muscarinic acetylcholine receptor m2 , muscarinic acetylcholine receptor m5 , muscarinic agonist , acetylcholine receptor , agonist , biophysics , pharmacology , endocrinology , receptor , biochemistry , biology
Activation of Torpedo presynaptic muscarinic acetylcholine (ACh) receptors with the agonist oxotremorine (20 μM) results in the inhibition of Ca 2+ ‐dependent release of endogenous ACh from Torpedo synaptosomes. This effect is reversed by the muscarinic antagonist atropine (1 μM) which, by itself, has no effect. In contrast, under the same conditions the amount of newly synthesized radiolabeled [ 3 H]ACh released is not affected by muscarinic ligands. These findings suggest that presynaptic muscarinic inhibition in the Torpedo is due to interference with the mobilization of ACh from a storage pool.