Bournaud R, Mallart A
Muscle Nerve. 1987 Jan;10(1):1-5. doi: 10.1002/mus.880100103.
An electrophysiologic study has been performed on motor nerves of mice affected with hereditary "motor endplate disease" (MED). Bath application of potassium channel blockers, such as tetraethylammonium and 3,4-diaminopyridine, which are almost without effect on the monophasic compound action potential of normal nerves, considerably enhanced the action potential duration in nerves from mutant mice. Furthermore, external current recordings from motor endings revealed an absence of the K-dependent waveform component in MED mice, which indicates a similar K current intensity in the terminal part of the endings and in the heminode. These observations suggest that in the mutant, unlike in normal mice, K channels play a role in action potential electrogenesis. Possible relationships with paranodal dysmyelination are discussed.
对患有遗传性“运动终板病”（MED）的小鼠运动神经进行了电生理研究。浴用钾通道阻滞剂，如几乎对正常神经的单相复合动作电位无影响的四乙铵和3,4-二氨基吡啶，可显著延长突变小鼠神经的动作电位持续时间。此外，运动终末的外部电流记录显示，MED小鼠缺乏K依赖性波形成分，这表明终末部分和半结中的K电流强度相似。这些观察结果表明，与正常小鼠不同，在突变体中，K通道在动作电位的电发生中起作用。文中还讨论了与结旁脱髓鞘的可能关系。
