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Effects of Pertussis Toxin Suggest a Role for G‐Proteins in the Inhibition of Acetylcholine Release from Rat Myenteric Plexus by Opioid and Presynaptic Muscarinic Receptors
Author(s) -
Doležal V.,
Tuček S.,
Hynie S.
Publication year - 1989
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1989.tb00779.x
Subject(s) - myenteric plexus , muscarinic acetylcholine receptor , acetylcholine , pertussis toxin , chemistry , (+) naloxone , tetrodotoxin , depolarization , endocrinology , medicine , pharmacology , receptor , opioid , g protein , biology , biochemistry , immunohistochemistry
Abstract1 Longitudinal muscle preparations of the rat ileum with the attached myenteric plexuses (LMMPs) were preloaded with (3H)choline and the effects of drugs on the depolarization‐evoked release of radioactivity corresponding to ( 3 H) acetylcholine (( 3 H)ACh) were measured. The release of ( 3 H)ACh was inhibited by morphine and the effect of morphine was blocked by naloxone. Morphine had no effect on the release of ( 3 H)ACh in LMMPs from rats that had been injected with pertussis toxin (PTX) 7 days before experiments. 2 Carbamoylcholine applied in the presence of tetrodotoxin inhibited the release of ( 3 H)ACh evoked by depolarization of LMMPs. The effect of carbamoylcholine was absent in LMMPs from rats pretreated with PTX. 3 The effects of PTX indicate that one or more PTX‐sensitive G proteins are involved in the chain of events mediating the action of opioid and muscarinic receptors on the release of ACh from the myenteric plexus. It is suggested that the inhibition of ACh release depends on G‐protein‐mediated coupling of opiod receptors with K + channels and of muscarinic receptors with Ca 2+ channels, but alternative explanations cannot be excluded.