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丁卡因对青蛙骨骼肌延迟钾通道和位移电流的不同作用。

Differential effects of tetracaine on delayed potassium channels and displacement currents in frog skeletal muscle.

作者信息

Almers W

出版信息

J Physiol. 1976 Nov;262(3):613-37. doi: 10.1113/jphysiol.1976.sp011612.

Abstract
  1. Delayed K+-currents and displacement currents were studied with a voltage-clamp technique. 2. In normal fibres, the conductance of the delayed channel grows e-fold per 3 millivolts at sufficiently negative potentials and reaches a limiting value of 2-10 m-mho/cm2 (mean 5-8 m-mho/cm2) at positive potentials. Adding tetracaine (2 mM) reduces the limiting conductance, shifts the voltage-dependence of the delayed channel to +25 mV more positive potentials and slows the kinetics fourfold. 3. By contrast, the displacement currents are virtually unaltered by 2 mM tetracaine. Their voltage-dependence is shifted by less than 5 mV and their kinetics are unaffected. 4. Tetraethylammonium ions (TEA) are known to slow the kinetics of delayed K+-channels fivefold but fail, like tetracaine, to change the kinetics of the displacement currents. 5. Both tetracaine and TEA have thus large effects on the 'gating' of the delayed channel, yet little or none on the displacement currents. This suggests that the displacement currents in skeletal muscle are for the most part unrelated to the opening and closing of delayed channels. It is estimated that 'gating' the delayed channel in muscle may require no more than 1 or 2% of the observed charge displacement.
摘要
  1. 采用电压钳技术研究延迟钾电流和位移电流。2. 在正常纤维中,延迟通道的电导在足够负的电位下每3毫伏增加一倍,并在正电位下达到2 - 10毫姆欧/平方厘米的极限值(平均5 - 8毫姆欧/平方厘米)。加入丁卡因(2毫摩尔)会降低极限电导,使延迟通道的电压依赖性向更正的电位移动25毫伏,并使动力学减慢四倍。3. 相比之下,2毫摩尔丁卡因对位移电流几乎没有影响。它们的电压依赖性移动小于5毫伏,并且它们的动力学不受影响。4. 已知四乙铵离子(TEA)会使延迟钾通道的动力学减慢五倍,但与丁卡因一样,不会改变位移电流的动力学。5. 因此,丁卡因和TEA对延迟通道的“门控”都有很大影响,但对位移电流几乎没有影响。这表明骨骼肌中的位移电流在很大程度上与延迟通道的开放和关闭无关。据估计,肌肉中延迟通道的“门控”可能只需要不超过观察到的电荷位移的1%或2%。

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