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Barium resistant potassium current in mammalian skeletal muscle following denervation.

机译:失神经后哺乳动物骨骼肌中的钡抗钾电流。

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Inward rectifier potassium channels are thought to be related to resting membrane potential and in innervated skeletal muscle they are specially sensitive to the blocking action of Ba2+ ions. After denervation other channels are known to become resistant to their blockers. We study the effect of Ba2+ upon the inward rectifier potassium channels after denervation. Rat extensor digitorum longus fibers were equilibrated for 150 minutes in 150 mM KCl; when they were returned to 5 mM KCl the resting potential went back to its original level with a half time of 35 minutes. This repolarization was blocked by 5 mM BaCl2 in innervated muscles and in muscles denervated for 7 days, but failed to do so after 14 days of denervation. Voltage-clamp experiments performed in lumbricalis denervated muscle showed a lack of effect of Ba2+ upon potassium current after 18 days of denervation. This results suggest that the inward rectifier potassium channels become resistant to Ba2+ ions after denervation, indicating a neural influence.
机译:内向整流钾通道被认为与静息膜电位有关,在神经支配的骨骼肌中,它们对Ba2 +离子的阻断作用特别敏感。取消神经支配后,其他通道会对其阻滞剂产生抵抗力。我们研究了去神经后Ba2 +对内向整流钾通道的影响。大鼠伸指长肌纤维在150 mM KCl中平衡150分钟。当将它们恢复到5 mM KCl时,静置电位在35分钟的一半时间内恢复到原始水平。受神经支配的肌肉和经神经支配的肌肉中7天的5 mM BaCl2阻止了这种复极化,但在神经支配14天后未能这样做。在去神经支配神经的肌肉中进行的电压钳实验显示,去神经支配18天后,Ba2 +对钾电流缺乏影响。该结果表明,去神经作用后,内向整流钾通道对Ba2 +离子具有抗性,表明存在神经影响。

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