Premium
Release of acetylcholine at the motor endplate of the rat — evidence against a muscarinic acetylcholine autoreceptor
Author(s) -
Häggblad J.,
Heilbronn E.
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb10717.x
Subject(s) - muscarinic acetylcholine receptor , acetylcholine , atropine , chemistry , endocrinology , medicine , muscarinic acetylcholine receptor m4 , physostigmine , autoreceptor , cholinergic , muscarinic acetylcholine receptor m2 , oxotremorine , muscarinic acetylcholine receptor m5 , muscarinic acetylcholine receptor m3 , biology , receptor , biochemistry , antagonist
1 The effect of some drugs on the release of endogenous acetylcholine from the phrenic nerve‐hemidiaphragm preparation of the rat was measured. Muscarinic ligands had no effect. 8‐Br‐cyclic GMP, a penetrating analogue of cyclic guanosine 3′,5′‐monophosphate (cyclic GMP) was also without effect. 8‐Br‐cyclic AMP somewhat enhanced the basal release while the potassium‐induced release remained unaltered. 2 In supersensitivity experiments, no specific binding of ligand [ 3 H]‐quinuclidinylbenzilate ([ 3 H]‐QNB) was found in homogenates of the diaphragm, either before or after atropine treatment, while concomitant binding studies in the CNS demonstrated the expected increase in muscarinic binding sites after atropine. 3 Our conclusion is that muscarinic acetylcholine receptors are probably absent from the presynaptic motor endplate area of the rat. Certain preliminary results suggest that a presynaptic nicotinic mechanism might be involved in the release of acetylcholine.