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高氯酸盐可增强骨骼肌兴奋-收缩偶联中的信号传递。

Perchlorate enhances transmission in skeletal muscle excitation-contraction coupling.

作者信息

González A, Ríos E

机构信息

Department of Physiology, Rush University School of Medicine, Chicago, Illinois 60612.

出版信息

J Gen Physiol. 1993 Sep;102(3):373-421. doi: 10.1085/jgp.102.3.373.

Abstract

The effects of the anion perchlorate (present extracellularly at 8 mM) were studied on functional skeletal muscle fibers from Rana pipiens, voltage-clamped in a Vaseline gap chamber. Established methods were used to monitor intramembranous charge movement and flux of Ca release from the sarcoplasmic reticulum (SR) during pulse depolarization. Saponin permeabilization of the end portions of the fiber segment (Irving, M., J. Maylie, N. L. Sizto, and W. K. Chandler. 1987. Journal of General Physiology. 89:1-41) substantially reduced the amount of charge moving during conventional control pulses, thus minimizing a technical error that plagued our previous studies. Perchlorate prolonged the ON time course of charge movement, especially at low and intermediate voltages. The OFFs were also made slower, the time constant increasing twofold. The hump kinetic component was exaggerated by ClO4- or was made to appear in fibers that did not have it in reference conditions. ClO4- had essentially no kinetic ON effects at high voltages (> or = 10 mV). ClO4- changed the voltage distribution of mobile charge. In single Boltzmann fits, the midpoint potential V was shifted -20 mV and the steepness parameter K was reduced by 4.7 mV (or 1.78-fold), but the maximum charge was unchanged (n = 9). Total Ca content in the SR, estimated using the method of Schneider et al. (Schneider, M. F., B. J. Simon, and G. Szucs. 1987. Journal of Physiology. 392:167-192) for correcting for depletion, stayed constant over tens of minutes in reference conditions but decayed in ClO4- at an average rate of 0.3 mumol/liter myoplasmic water per s. ClO4- changed the kinetics of release flux, reducing the fractional inactivation of release after the peak. ClO4- shifted the voltage dependence of Ca release flux. In particular, the threshold voltage for Ca release was shifted by about -20 mV, and the activation of the steady component of release flux was shifted by > 20 mV in the negative direction. The shift of release activation was greater than that of mobile charge. Thus the threshold charge, defined as the minimum charge moved for eliciting a detectable Ca transient, was reduced from 6 nC/microF (0.55, n = 7) to 3.4 (0.53). The average of the paired differences was 2.8 (0.33, P < 0.01). The effects of ClO4- were then studied in fibers in modified functional situations. Depletion of Ca in the SR, achieved by high frequency pulsing in the presence of intracellular BAPTA and EGTA, simplified but did not eliminate the effects of ClO4-.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

研究了细胞外浓度为8 mM的阴离子高氯酸盐对牛蛙功能性骨骼肌纤维的影响,这些纤维在凡士林间隙室中进行电压钳制。采用既定方法监测脉冲去极化期间膜内电荷移动和肌浆网(SR)钙释放通量。用皂角苷通透纤维段的末端部分(欧文,M.,J. 梅利,N. L. 西兹托,和W. K. 钱德勒。1987年。《普通生理学杂志》。89:1 - 41),显著减少了传统对照脉冲期间移动的电荷量,从而将困扰我们先前研究的技术误差降至最低。高氯酸盐延长了电荷移动的开启时间进程,尤其是在低电压和中等电压时。关闭时间也变慢,时间常数增加了两倍。驼峰动力学成分被高氯酸根离子夸大,或者在对照条件下没有该成分的纤维中显现出来。高氯酸盐在高电压(≥10 mV)时基本上没有动力学开启效应。高氯酸盐改变了可移动电荷的电压分布。在单玻尔兹曼拟合中,中点电位V向负方向移动了20 mV,陡度参数K降低了4.7 mV(或1.78倍),但最大电荷量不变(n = 9)。使用施耐德等人(施耐德,M. F.,B. J. 西蒙,和G. 苏茨。1987年。《生理学杂志》。392:167 - 192)的方法校正耗竭后估算的SR中总钙含量,在对照条件下几十分钟内保持恒定,但在高氯酸盐存在下以平均每秒0.3 μmol/升肌浆水的速率衰减。高氯酸盐改变了释放通量的动力学,降低了峰值后释放的分数失活。高氯酸盐使钙释放通量的电压依赖性发生了偏移。特别是,钙释放的阈值电压向负方向偏移了约20 mV,释放通量稳定成分的激活向负方向偏移了超过20 mV。释放激活的偏移大于可移动电荷的偏移。因此,定义为引发可检测钙瞬变所需移动的最小电荷量的阈值电荷,从6 nC/μF(0.55,n = 7)降至3.4(0.53)。配对差异的平均值为2.8(0.33,P < 0.01)。然后在改变功能状态的纤维中研究了高氯酸盐的作用。通过在细胞内BAPTA和EGTA存在下高频脉冲实现SR中钙的耗竭,简化但并未消除高氯酸盐的作用。(摘要截于400字)

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