低频刺激大鼠快缩肌单纤维钙瞬变。

S Carroll, P Nicotera, D Pette
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引用次数: 64

摘要

研究了大鼠指长伸肌在不同时间(10天)的慢性低频刺激下的Ca(2+)瞬态。在刺激开始后2小时,观察到静息Ca(2+)浓度([Ca(2+)])增加约2.5倍,并在整个刺激期间持续。升高的[Ca(2+)]水平在比目鱼肌慢肌纤维的特征范围内。此外,我们注意到每脉冲积分[Ca(2+)]的短暂升高,在1天后达到最大值(约5倍)。[Ca(2+)]衰变速率常数的急剧下降可以解释为Ca(2+)摄取的直接损害,并且随着刺激周期的延长,由于小蛋白含量的衰减导致细胞质Ca(2+)结合能力的额外损失。在10天的刺激肌肉中,[Ca(2+)]衰变速率常数的部分恢复可以通过增加线粒体对Ca(2+)封存的贡献来解释。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Calcium transients in single fibers of low-frequency stimulated fast-twitch muscle of rat.

Ca(2+) transients were investigated in single fibers isolated from rat extensor digitorum longus muscles exposed to chronic low-frequency stimulation for different time periods up to 10 days. Approximately 2.5-fold increases in resting Ca(2+) concentration ([Ca(2+)]) were observed 2 h after stimulation onset and persisted throughout the stimulation period. The elevated [Ca(2+)] levels were in the range characteristic of slow-twitch fibers from soleus muscle. In addition, we noticed a transitory elevation of the integral [Ca(2+)] per pulse with a maximum ( approximately 5-fold) after 1 day. Steep decreases in rate constant of [Ca(2+)] decay could be explained by an immediate impairment of Ca(2+) uptake and, with longer stimulation periods, by an additional loss of cytosolic Ca(2+) binding capacity resulting from a decay in parvalbumin content. A partial recovery of the rate constant of [Ca(2+)] decay in 10-day stimulated muscle could be explained by an increasing mitochondrial contribution to Ca(2+) sequestration.

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