[Nonquantum release of acetylcholine in frog neuromuscular junction after blocking of axoplasmic transport with colchicine].
Standard microelectrode techniques were used to evaluate the effect of d-tubocurarine chloride on membrane potential of junctional and extrajunctional areas of muscle fibers in a potassium-free Ringer solution. The experiments were made on frogs after inactivation of acetylcholinesterase. d-Tubocurarine chloride hyperpolarized the membrane of muscle fibers only in the junctional area. Blockade of axoplasmic transport with colchicine did not affect the magnitude of the hyperpolarization response of the membrane end plate to the presence of d-tubocurarine chloride, but at the same time it significantly reduced the membrane rest potential of muscle fibers, and gave rise to the appearance of extrajunctional sensitivity to acetylcholine. It is concluded that the blockade of axoplasmic transport does not affect the pattern of non-quantum acetylcholine release from nerve terminals. Therefore, this is unlikely to cause denervation-like changes in the muscle under the conditions described.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001138:Armin / Q000494:pharmacology; D001370:Axonal Transport / Q000187:drug effects*; D003078:Colchicine / Q000494:pharmacology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009469:Neuromuscular Junction / Q000502:physiology*; D011895:Rana ridibunda; D013570:Synaptic Membranes / Q000502:physiology; D014403:Tubocurarine / Q000494:pharmacology
D001138:Armin; D000109:Acetylcholine; D003078:Colchicine; D014403:Tubocurarine
Nekvantovyĭ vykhod atsetilkholina v mionevral'nom soedinenii liagushki posle narusheniia aksoplasmaticheskogo transporta kolkhitsinom.