[Mechanism of carbachol and adenosine action on spontaneous quantal mediator release at frog neuromuscular junction].
Experiments on the frog sartorius muscle showed that nonhydrolisable acetylcholine analog carbachol (CCh) depresses spontaneous quantal mediator release via muscarinic M2 receptors of nerve ending. Adenosine (Ade) acting via inhibitory A1 receptors is another strong spontaneous quantal release modulator. Inhibition of pertussis toxin (PTx)-sensitive G-proteins only partly eliminated CCh and Ade depressive action. It means metabotropic A1 and M2 receptors of the frog nerve ending regulate spontaneous quantal release via activating of both PTx-sensitive and PTx-insensitive inhibitory mechanisms.
Shakirzianova
A V
AV
Bukharaeva
E A
EA
Giniatullin
R A
RA
Nikol'skiĭ
E E
EE
D000241:Adenosine / Q000494:pharmacology*; D058907:Adenosine A1 Receptor Agonists; D000818:Animals; D002217:Carbachol / Q000494:pharmacology*; D019204:GTP-Binding Proteins / Q000037:antagonists & inhibitors; D008564:Membrane Potentials; D018482:Muscle, Skeletal / Q000187:drug effects; D009411:Nerve Endings / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000378:metabolism*; D037342:Pertussis Toxin / Q000494:pharmacology; D011895:Rana ridibunda; D043585:Receptor, Muscarinic M2 / Q000819:agonists; D009435:Synaptic Transmission / Q000187:drug effects
D058907:Adenosine A1 Receptor Agonists; D043585:Receptor, Muscarinic M2; D002217:Carbachol; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins; D000241:Adenosine