[Neurotrophic control of the resting membrane potential of phasic muscle fibers in frogs].
Muscle denervation or blockade of axoplasmic transport by colchicine with no impairment of neuro-muscular transmission, cause a decrease of the resting membrane potential (RMP) of muscle fibers in frogs. Administration of actinomycin D or puromycin does not affect the development of depolarization in muscle fibers under these conditions. Ouabain does not change the RMP of muscle fibers, which indicates to small amount of "pumping" current in the RMP. Adrenaline, insulin, dibutyryl c. AMP, theophylline hyperpolarize the muscle fiber membrane in denervated and intact muscles. Ouabain abolishes this effect. The fiber RMP in denervated and colchicine treated muscles in potassium-free Ringer solution is lower than in intact muscles under similar conditions. The mechanism of postdenervation depolarization of muscle fibers seems to depend on decrease in the intact intracellular potassium concentration as a result of Na+, K+-pump diminished activity. Neurotrophic control of muscle fibers RMP in frog depends on the substances supplied by axoplasmic flow.
D000818:Animals; D002463:Cell Membrane Permeability; D004837:Epinephrine / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D008564:Membrane Potentials; D009121:Muscle Denervation; D009132:Muscles / Q000378:metabolism / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D011896:Rana temporaria; D012964:Sodium / Q000378:metabolism*
D007328:Insulin; D012964:Sodium; D011188:Potassium; D004837:Epinephrine
Neĭrotroficheskiĭ kontrol'membrannogo potentsiala pokoia faznykh myshechnykh volokon liagushki.