EFFECTS OF EXTRACELLULAR CALCIUM ON CALCIUM MOVEMENTS OF EXCITATION CONTRACTION COUPLING IN FROG SKELETAL-MUSCLE FIBERS
EFFECTS OF EXTRACELLULAR CALCIUM ON CALCIUM MOVEMENTS OF EXCITATION CONTRACTION COUPLING IN FROG SKELETAL-MUSCLE FIBERS
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DOI：
10.1113/jphysiol.1988.sp017052
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发表时间：
1988-04-01
影响因子：
5.5
通讯作者：
STEFANI, E
中科院分区：
文献类型：
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作者：
BRUM, G;RIOS, E;STEFANI, E
1.在电压钳制的双缝室中，研究了低细胞外游离钙离子浓度（Ca ~（2+））对与膜去极化相关的胞浆[Ca ~（2+）]瞬时变化（Ca ~（2+）瞬态）的影响。用细胞内扩散的染料Antiyprylazo III监测Ca 2+瞬变。2.在低[Ca 2 +]（10-5 M或更低，Mg 2+取代Ca 2+）的外部盐水中，Ca 2+瞬变大大减少。这种降低在100 ms或更长去极化脉冲期间的后期更明显。3.低[Ca ~（2+）]o并不改变从肌浆溶液中去除Ca ~（2+）的过程速率。这意味着Ca ~（2+）进入肌浆的输入通量减少。4.肌浆网（SR）释放的Ca ~（2+）流量加上T-小管膜Ca ~（2+）通道的Ca ~（2+）内流，即Ca ~（2+）输入流量。在低[Ca 2 +]o的峰值输入通量减少了45%（n = 16纤维），衰减更迅速，在去极化脉冲。5.由于[Ca 2 +]o减少导致的通过T-小管膜Ca 2+通道的Ca 2+内流的减少不能解释超过Ca 2+输入通量减少的5%，因此将其解释为SR释放的实际减少。内向（T-管）Ca 2+电流与细胞外Ca 2+的这种效应无关，因为这种效应在高细胞内电压下是电压无关的，在高细胞内电压下，Ca 2+内向电流是强烈的电压依赖性。7.低[Ca 2 +]o使Ca 2+释放更容易失活;低[Ca 2 +]o的影响最好描述为Ca 2+释放的“失活曲线”左移29 mV，将峰值释放通量与膜保持电位相关联。8.由低[Ca 2 +]o引起的Ca 2+释放的减少并不伴随着Ca 2+释放的电压依赖性或刚好可检测释放的阈值电压的变化。9.这一结果与Ca ~（2+）对兴奋-收缩耦联的T管膜电压传感器的主要作用一致。
1. The effect of low extracellular free calcium ion concentration (Ca2+]o) on the transient changes in cytoplasmic [Ca2+] associated with membrane depolarization (Ca2+ transients) was studied on single cut skeletal muscle fibres of the frog, voltage clamped in a double-Vaseline-gap chamber. The Ca2+ transients were monitored with the dye Antiyprylazo III diffused intracellularly. 2. The Ca2+ transients were substantially reduced in external salines with low [Ca2+] (10-5 M or less and Mg2+ substituted for Ca2+). This decrease was more noticeable at late times during 100 ms or longer depolarizing pulses. 3. The rates of the processes that remove Ca2+ from the myoplasmic solution were not altered by the low [Ca2+]o. This implies that the input flux of Ca2+ into the myoplasm was reduced. 4. The Ca2+ input flux, equal to release flux from the sarcoplasmic reticulum (SR) plus Ca2+ influx via the T-tubule membrane Ca2+ channel, was derived from the Ca2+ transient. In low [Ca2+]o the peak input flux was reduced by 45% (n = 16 fibres) and decayed more rapidly during a depolarizing pulse. 5. The reduction in Ca2+ influx via the T-tubule membrane Ca2+ channel due to the reduced [Ca2+]o could not account for more than 5% of the reduction in Ca2+ input flux, which was thus interpreted as an actual reduction of release from the SR. 6. The inward (T-tubular) Ca2+ current was not associated with this effect of extracellular Ca2+ as the effect was voltage independent at high intracellular voltages at which the Ca2+ inward current was strongly voltage dependent. 7. Low [Ca2+]o made Ca2+ release more readily inactivatable; the effect of low [Ca2+]o is best described as a left shift by 29 mV of the ''inactivation curve'' of Ca2+ release, relating peak release flux to membrane holding potential. 8. The reduction of Ca2+ release by low [Ca2+]o was not accompanied by changes in the voltage dependence of Ca2+ release or in the threshold voltage for just-detectable release. 9. The results are consistent with a primary effect of Ca2+ on the T-tubular-membrane voltage sensor of excitation-contraction coupling.