Hui Chiu Shuen
Department of Cellular and Integrative Physiology, Indiana University Medical Center, Indianapolis, IN 46202, USA.
Biophys J. 2005 Feb;88(2):1030-45. doi: 10.1529/biophysj.104.048215. Epub 2004 Nov 8.
Charge movement and calcium transient were measured simultaneously in stretched frog cut twitch fibers under voltage clamp, with the internal solution containing 20 mM EGTA plus added calcium and antipyrylazo III. When the nominal free [Ca2+]i was 10 nM, the shape of the broad I(gamma) hump in the ON segments of charge movement traces remained invariant when the calcium release rate was greatly diminished. When the nominal free [Ca2+]i was 50 nM, which was close to the physiological level, the I(gamma) humps were accelerated and a slow calcium-dependent I(delta) component (or state) was generated. The peak of ON I(delta) synchronized perfectly with the peak of the calcium release rate whereas the slow decay of ON I(delta) followed the same time course as the decay of calcium release rate. Suppression of calcium release by TMB-8 reduced the amount of Q(delta) concomitantly but not completely, and the effects were partially reversible. The same simultaneous suppression effects were achieved by depleting the sarcoplasmic reticulum calcium store with repetitive stimulation. The results suggest that the mobility of Q(delta) needs to be primed by a physiological level of resting myoplasmic Ca2+. Once the priming is completed, more I(delta) is mobilized by the released Ca2+ during depolarization.
在电压钳制下，对拉伸的青蛙离体单收缩纤维同时测量电荷移动和钙瞬变，内部溶液含有20 mM乙二醇双四乙酸（EGTA）外加钙和安替比拉佐III。当名义游离[Ca2+]i为10 nM时，电荷移动轨迹开启段中宽的I(γ)峰的形状在钙释放速率大幅降低时保持不变。当名义游离[Ca2+]i为50 nM（接近生理水平）时，I(γ)峰加速，并且产生了一个缓慢的钙依赖性I(δ)成分（或状态）。开启I(δ)的峰值与钙释放速率的峰值完美同步，而开启I(δ)的缓慢衰减与钙释放速率的衰减遵循相同的时间进程。四甲基联苯胺（TMB - 8）抑制钙释放会相应地但并非完全地减少Q(δ)的量，并且这些效应部分可逆。通过重复刺激耗尽肌浆网钙储存也能产生相同的同时抑制效应。结果表明，Q(δ)的迁移率需要由静息肌浆Ca2+的生理水平引发。一旦引发完成，在去极化过程中更多的I(δ)会被释放的Ca2+动员起来。
