Long-term depolarization regulates the alpha1s, subunit of skeletal muscle Ca2+ channels and the amplitude of L-type Ca2+ currents.
Long-term depolarization regulates the alpha1s, subunit of skeletal muscle Ca2+ channels and the amplitude of L-type Ca2+ currents.
复制标题
长期去极化调节 α1、骨骼肌 Ca2 通道亚基和 L 型 Ca2 电流的幅度。
DOI：
10.1007/s004240100606
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Sánchez,JA
中科院分区：
文献类型：
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作者：
Escamilla,J;Farías,JM;García,R;García,MC;Sánchez,JA
研究了长期去极化对骨骼肌L型Ca2+电流α1sand水平的影响。蛋白质印迹技术显示，长期去极化（14 小时）导致 α1 减少 50%。通过与 Ca2+ 通道阻滞剂硝苯地平预孵育可以防止这种下降。使用电压钳技术进行电生理学实验来测量长期去极化对 Ca2+ 电流和电荷运动的作用。观察到持续 0.5-14 小时的去极化导致 Ca2+ 电流幅度逐渐下降。与Western blot结果类似，硝苯地平可以阻止电流幅度的下降，并且它依赖于外部Ca2+。长期去极化也显着减少了由阶跃脉冲调动的非线性电荷（50%）。表明α1s亚基通过非常严格的机制通过长期去极化而下调，并且在此过程中，通过L型通道渗透的Ca2+离子发挥了关键作用。提出了 L 型 Ca2+ 电流在骨骼肌纤维中的新作用，其中通道是自我调节的。
The effects of long-term depolarization on the level of α1sand on L-type Ca2+currents of skeletal muscle were investigated. Long-term depolarization (14 h) caused a 50% decrease of α1s, revealed with the Western blot technique. This decline was prevented by preincubation with the Ca2+channel blocker nifedipine. Electrophysiological experiments using the voltage-clamp technique were performed to measure the actions of long-term depolarization on Ca2+currents and charge movement. A progressive decline in the amplitude of the Ca2+currents by depolarizations lasting 0.5–14 h was observed. Similar to Western blot results, the fall in current amplitude was prevented by nifedipine, and it depended on external Ca2+. The nonlinear charge mobilized by step pulses was also significantly reduced (50%) by long-term depolarization. It is suggested that α1ssubunit is down-regulated by long-term depolarization by a very stringent mechanism and that, in this process, Ca2+ions permeating through L-type channels play a key role. A new role for the L-type Ca2+current in skeletal muscle fibers in which the channels are self-regulated is proposed.