[Non-quantum secretion of acetylcholine in a nerve-muscle preparation of the diaphragm in dystrophic mice of line 129/Rej].
Experiments were carried out on phenotypically normal and sick homozygotic 129/Rej mice suffering from congenital dystrophy. The membrane rest potential (MRP) for muscle fibers of sick homozygotic animal diaphragm appeared lower than that of phenotypically normal species, attesting to the denervation-like pattern of muscle pathology. After muscle treatment with armine, and irreversible acetylcholinesterase inhibitor, d-tubocurarine chloride hyperpolarized the postsynaptic membrane without affecting the MRP of the extrasynaptic zone of muscle fibers. The magnitude of the postsynaptic hyperpolarization of the muscle membrane in response to curare turned out to be the same in both phenotypically normal and sick homozygotic mice. It is suggested that the genetic defect in question does not change the pattern of non-quantum acetylcholine secretion from the motor nerve endings. Therefore, this cannot be the reason for muscle pathology.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001138:Armin / Q000494:pharmacology; D003964:Diaphragm; D006720:Homozygote; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009137:Muscular Dystrophy, Animal / Q000235:genetics* / Q000378:metabolism; D009469:Neuromuscular Junction / Q000187:drug effects / Q000378:metabolism*; D014403:Tubocurarine / Q000494:pharmacology
D001138:Armin; D000109:Acetylcholine; D014403:Tubocurarine
Nekvantovyĭ vykhod atsetilkholina v nervno-myshechnom preparate diafragmy distrofichnykh mysheĭ linii 129/Rej.