Chua M, Dulhunty A F
Department of Physiology, John Curtin School of Medical Research, Australian National University, Canberra.
J Gen Physiol. 1989 Jul;94(1):183-203. doi: 10.1085/jgp.94.1.183.
Inactivation of excitation-contraction coupling was examined in extensor digitorum longus (EDL) and soleus muscle fibers from rats injected daily with tri-iodothyronine (T3, 150 micrograms/kg) for 10-14 d. Steady-state activation and inactivation curves for contraction were obtained from measurements of peak potassium contracture tension at different surface membrane potentials. The experiments tested the hypothesis that noninactivating tension is a "window" tension caused by the overlap of the activation and inactivation curves. Changes in the amplitude and voltage dependence of noninactivating tension should be predicted by the changes in the activation and inactivation curves, if noninactivating tension arises from their overlap. After T3 treatment, the area of overlap increased in EDL fibers and decreased in soleus fibers and the overlap region was shifted to more negative potentials in both muscles. Noninactivating tension also appeared at more negative membrane potentials after T3 treatment in both EDL and soleus fibers. The effects of T3 treatment were confirmed with a two microelectrode voltage-clamp technique: at the resting membrane potential (-80 mV) contraction in response to a brief test pulse required less than normal depolarization in EDL, but more than normal depolarization in soleus fibers. After T3 treatment, the increase in contraction threshold at depolarized holding potentials (attributed to inactivation) occurred at more depolarized holding potentials in EDL, or less depolarized holding potentials in soleus. The changes in contraction threshold could be accounted for by the effects of T3 on the activation and inactivation curves. In conclusion, (a) T3 appeared to affect the expression of both activation and inactivation characteristics, but the activation effects could not be cleanly distinguished from T3 effects on the sarcoplasmic reticulum and contractile proteins, and (b) the experiments provided evidence for the hypothesis that the noninactivating tension is a steady-state "window" tension.
对每日注射三碘甲状腺原氨酸（T3，150微克/千克）10 - 14天的大鼠的趾长伸肌（EDL）和比目鱼肌纤维中的兴奋 - 收缩偶联失活进行了研究。通过测量不同表面膜电位下的峰值钾挛缩张力，获得了收缩的稳态激活和失活曲线。实验检验了这样一个假设，即非失活张力是由激活曲线和失活曲线重叠引起的“窗口”张力。如果非失活张力源于它们的重叠，那么非失活张力的幅度和电压依赖性变化应该可以通过激活曲线和失活曲线的变化来预测。T3处理后，EDL纤维中的重叠面积增加，比目鱼肌纤维中的重叠面积减少，并且重叠区域在两块肌肉中都向更负的电位移动。T3处理后，EDL和比目鱼肌纤维在更负的膜电位下也出现了非失活张力。用双微电极电压钳技术证实了T3处理的效果：在静息膜电位（-80 mV）下，对短暂测试脉冲的收缩反应在EDL中所需的去极化小于正常，而在比目鱼肌纤维中则大于正常。T3处理后，去极化钳制电位下收缩阈值的增加（归因于失活）在EDL中出现在更高的去极化钳制电位，或在比目鱼肌中出现在更低的去极化钳制电位。收缩阈值的变化可以用T3对激活曲线和失活曲线的影响来解释。总之，（a）T3似乎影响激活和失活特征的表达，但激活效应无法与T3对肌浆网和收缩蛋白的效应清晰区分，并且（b）实验为非失活张力是稳态“窗口”张力这一假设提供了证据。
