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Muscarine Receptors Regulating Electrically Evoked Release of Acetylcholine in Hippocampus Are Linked to Pertussis Toxin‐Sensitive G Proteins but Not to Adenylate Cyclase
Author(s) -
Allgaier Clemens,
Choi Bong Kyo,
Hertting Georg
Publication year - 1993
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.1471-4159.1993.tb03618.x
Subject(s) - oxotremorine , muscarine , pertussis toxin , muscarinic acetylcholine receptor , chemistry , carbachol , endocrinology , medicine , acetylcholine , cholera toxin , muscarinic acetylcholine receptor m5 , cyclase , g protein , muscarinic acetylcholine receptor m2 , agonist , receptor , muscarinic acetylcholine receptor m3 , biology , biochemistry
[ 3 H]Acetylcholine release elicited with 360 pulses/3 Hz from slices of rabbit hippocampus is facilitated in the presence of the muscarine (M) receptor antagonist atropine (indicating the existence of autoinhibition) and diminished by the M receptor agonists carbachol and oxotremorine. W‐Ethylmaleimide (30 μM ) and pertussis toxin (8 μg/ml) counteracted antagonist‐induced facilitation and agonist‐induced inhibition of release, suggesting that a pertussis toxin‐sensitive GTP‐binding protein is involved in the chain of events mediating activation of M receptors to inhibition of release. Neither 8‐bromo‐cyclic AMP (300 μM ), a membrane analogue of cyclic AMP, nor rolipram (10 μM ), a phosphodiesterase inhibitor, affected electrically evoked release of [ 3 H]acetylcholine. They also did not influence the oxotremorine‐induced inhibition of transmitter release. In conclusion, no evidence was found for the assumption that activation of M autoreceptors is linked to inhibition of adenylate cyclase.