Hui C S, Milton R L
J Muscle Res Cell Motil. 1987 Jun;8(3):195-208. doi: 10.1007/BF01574588.
Charge movements in intact frog twitch fibres were studied using a three-microelectrode voltage-clamp technique. When high potassium solution was applied transiently to the muscle fibres at low temperature in the presence of D600, the fibres became paralysed and, concomitantly, charge movement disappeared. The amount of charge suppressed by the paralysis treatment was about 70-100% of that in control experiments. This paralysing action of D600 is not shared by its derivative D890. The requirement of conditioning potassium contracture is, most likely, related to prolonged membrane depolarization, as voltage-clamped depolarization to 0 mV lasting tens of seconds also suppressed charge movement. When paralysed fibres were warmed, the main charge component (Q beta) was reprimed. By contrast, the hump charge component (Q gamma) was only reprimed in some of the fibres. Other than by warming, as paralysed fibre could be revived by stimulating it with large suprathreshold pulses but not by voltage-clamped hyperpolarization to -160 mV for tens of seconds. The paralysing action of D600 described here appears to be unrelated to its ability in blocking Ca2+ channels.
使用三微电极电压钳技术研究了完整青蛙抽搐纤维中的电荷移动。当在低温下于D600存在的情况下将高钾溶液短暂施加到肌肉纤维上时,纤维会麻痹,同时电荷移动消失。麻痹处理抑制的电荷量约为对照实验中电荷量的70 - 100%。D600的这种麻痹作用其衍生物D890并不具备。形成钾挛缩的条件要求很可能与长时间的膜去极化有关,因为将电压钳制在0 mV并持续数十秒也会抑制电荷移动。当麻痹的纤维升温时,主要电荷成分(Qβ)会重新被激发。相比之下,驼峰电荷成分(Qγ)仅在部分纤维中会重新被激发。除了升温外,麻痹的纤维可以通过用大的阈上脉冲刺激而恢复,但不能通过将电压钳制在 - 160 mV并持续数十秒来恢复。此处描述的D600的麻痹作用似乎与其阻断Ca2+通道的能力无关。