Jong D S, Pape P C, Baylor S M, Chandler W K
Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510-8026, USA.
J Gen Physiol. 1995 Aug;106(2):337-88. doi: 10.1085/jgp.106.2.337.
Cut muscle fibers from Rana temporaria (sarcomere length, 3.4-4.2 microns) were mounted in a double Vaseline-gap chamber (14-15 degrees C) and equilibrated with end-pool solutions that contained 20 mM EGTA and 1.76 mM Ca. Sarcoplasmic reticulum (SR) Ca release was estimated from changes in pH (Pape, P. C., D.-S. Jong, and W.K. Chandler. 1995. Journal of General Physiology. 106:000-000). Although the amplitude and duration of the [Ca] transient, as well as its spatial spread from the release sites, are reduced by EGTA, SR Ca release elicited by either depolarizing voltage-clamp pulses or action potentials behaved in a manner consistent with Ca inactivation of Ca release. After a step depolarization to -20 or 10 mV, the rate of SR Ca release, corrected for SR Ca depletion, reached a peak value within 5-15 ms and then rapidly decreased to a quasi-steady level that was about half the peak value; the time constant of the last half of the decrease was usually 2-4 ms. Immediately after an action potential or a 10-15 ms prepulse to -20 mV, the peak rate of SR Ca release elicited by a second stimulation, as well as the fractional amount of release, were substantially decreased. The rising phase of the rate of release was also reduced, suggesting that at least 0.9 of the ability of the SR to release Ca had been inactivated by the first stimulation. There was little change in intramembranous charge movement, suggesting that the changes in SR Ca release were not caused by changes in its voltage activation. These effects of a first stimulation on the rate of SR Ca release elicited by a second stimulation recovered during repolarization to -90 mV; the time constant of recovery was approximately 25 ms in the action-potential experiments and approximately 50 ms in the voltage-clamp experiments. Fura-2, which is able to bind Ca more rapidly than EGTA and hence reduce the amplitude of the [Ca] transient and its spatial spread from release sites by a greater amount, did not prevent Ca inactivation of Ca release, even at concentrations as large as 6-8 mM. These effects of Ca inactivation of Ca release can be simulated by the three-state, two-step model proposed by Schneider, M. F., and B. J. Simon (1988, Journal of Physiology. 405:727-745), in which SR Ca channels function as a single uniform population of channels. (ABSTRACT TRUNCATED AT 400 WORDS)
从林蛙(肌节长度为3.4 - 4.2微米)身上切下的肌肉纤维被安装在一个双凡士林间隙室(14 - 15摄氏度)中,并用含有20 mM乙二醇双四乙酸(EGTA)和1.76 mM钙的终池溶液进行平衡。根据pH值的变化来估计肌浆网(SR)的钙释放量(帕普,P.C.,D.-S. 钟,和W.K. 钱德勒。1995年。《普通生理学杂志》。106:000 - 000)。尽管EGTA会降低钙瞬变的幅度、持续时间以及其从释放位点的空间扩散,但由去极化电压钳脉冲或动作电位引发的SR钙释放的表现与钙释放的钙失活一致。在向 - 20或10 mV进行阶跃去极化后,校正了SR钙耗竭的SR钙释放速率在5 - 15毫秒内达到峰值,然后迅速下降到约为峰值一半的准稳态水平;下降后半段的时间常数通常为2 - 4毫秒。在动作电位或向 - 20 mV的10 - 15毫秒预脉冲之后,第二次刺激引发的SR钙释放的峰值速率以及释放的分数数量都大幅降低。释放速率的上升阶段也降低了,这表明SR释放钙的能力至少有0.9已被第一次刺激失活。膜内电荷移动几乎没有变化,这表明SR钙释放的变化不是由其电压激活的变化引起的。第一次刺激对第二次刺激引发的SR钙释放速率的这些影响在复极化到 - 90 mV期间恢复;在动作电位实验中恢复的时间常数约为25毫秒,在电压钳实验中约为50毫秒。与EGTA相比能够更快结合钙从而更大程度降低钙瞬变幅度及其从释放位点的空间扩散的Fura - 2,即使在浓度高达6 - 8 mM时也不能阻止钙释放的钙失活。钙释放的钙失活这些效应可以用施耐德,M.F.,和B.J. 西蒙(1988年,《生理学杂志》。405:727 - 745)提出的三态、两步模型来模拟,其中SR钙通道作为单一均匀的通道群体起作用。(摘要截取自400字)