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Colchicine alters apamin receptors, electrical activity, and skeletal muscle relaxation

机译:秋水仙碱改变阿帕明受体、电活动和骨骼肌松弛

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AbstractA low conductance calcium‐activated K+channel is thought to regulate the rate of firing of several excitable cells. In skeletal muscle the expression of this channel is under nerve control. Previously, we reported that axonal flow blockade of rat nerves, induced by colchicine, caused atransient increase in muscle apamin receptors, determined by125I‐apamin binding to membrane fractions. The increase in apamin receptors was correlated with repetitive discharges resembling myotonic potentials in the electromyogram, that were blockable by apamin. Here we show that the increase in muscle apamin receptors and the alteration of the electromyogram are followed closely by a slowing of the twitch relaxation, that in turn, is decreased by apamin. Furthermore, the presence of myotonic‐like alterations in the electromyogram and a slowing of muscle relaxation when muscle apaminreceptors are increased suggests that these channels may participate, amongother factors, in the generation of some kinds of myotonia. © 1993 John WileySon
机译:摘要低电导钙激活的K+通道被认为可以调节几种可兴奋细胞的放电速率。在骨骼肌中,该通道的表达受到神经控制。之前,我们报道了秋水仙碱诱导的大鼠神经轴突血流阻断,导致肌肉apamin受体的短暂增加,由125I-apamin与膜组分结合决定。apamin 受体的增加与肌电图中类似于强直电位的重复放电相关,这些放电可被 apamin 阻断。在这里,我们表明,肌肉apamin受体的增加和肌电图的改变紧随其后的是抽搐松弛的减慢,而抽搐松弛又被apamin减少。此外,肌电图中存在肌强直样改变,以及肌肉无骨素受体增加时肌肉松弛减慢,表明这些通道可能与其他因素一起参与某些类型的肌强直的产生。© 1993 约翰·威利父子

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