Volkov E M, Poletaev G I
Fiziol Zh SSSR Im I M Sechenova. 1981 Dec;67(12):1807-13.
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.
肌肉去神经支配或用秋水仙碱阻断轴浆运输(而不损害神经肌肉传递)会导致青蛙肌肉纤维静息膜电位(RMP)降低。在这些条件下,给予放线菌素D或嘌呤霉素不会影响肌肉纤维去极化的发展。哇巴因不会改变肌肉纤维的RMP,这表明RMP中存在少量“泵浦”电流。肾上腺素、胰岛素、二丁酰环磷腺苷、茶碱可使去神经和完整肌肉中的肌肉纤维膜超极化。哇巴因可消除这种作用。在无钾林格液中,去神经和用秋水仙碱处理的肌肉中的纤维RMP低于类似条件下的完整肌肉。肌肉纤维去神经后去极化的机制似乎取决于由于钠钾泵活性降低导致完整细胞内钾浓度降低。青蛙肌肉纤维RMP的神经营养控制取决于轴浆流提供的物质。