Müller-Mohnssen H, Tippe A, Hillenkamp F, Unsöld E
Z Naturforsch C Biosci. 1975 Mar-Apr;30(2):271-7.
The site of the pulse regeneration in myelinated nerve is generally assumed to be the unmyelinated part of the axon membrane in thr Ranvier node. To check this, a micro-irradiation technique using laser pulses (lambda equals 347 nm, t equals 20 ns) was used to produce morphological lesions of about 1 mum diameter in various regions of the Ranvier node. The electro-physiological functions were monitored parallel to the irradiation. Depending on the localizing of the lesions two types of changes in these functions were observed: 1. If a definite site in the paranodal myelin sheath was damaged without affecting the axon, an action potential could no longer be elicited, although the resting potential as well as the stationary current-voltage behaviour remained unchanged. 2. A damage of the axon resulted in a break down of membrane potential and resistance. In most of the cases the excitability recovered after spontaneous or current induced restitution of the membrane resting potential and resistance. These observations indicate, that structures in the paranodal region are vital for the Na+-activation and inactivation. The membrane potential and stationary current-voltage behavior can be attributed to the axon membrane. A new hypothesis concerning the mechanism of the Na+-activation-inactivation process is suggested.
一般认为,有髓神经中脉冲再生的部位是郎飞结处轴突膜的无髓鞘部分。为了验证这一点,使用一种利用激光脉冲(波长λ等于347纳米,脉宽t等于20纳秒)的微辐照技术,在郎飞结的不同区域产生直径约1微米的形态损伤。在辐照过程中同时监测电生理功能。根据损伤的定位,观察到这些功能有两种类型的变化:1. 如果结旁髓鞘的特定部位受损而不影响轴突,虽然静息电位以及静态电流 - 电压行为保持不变,但不再能引发动作电位。2. 轴突损伤导致膜电位和电阻崩溃。在大多数情况下,在膜静息电位和电阻自发恢复或电流诱导恢复后,兴奋性恢复。这些观察结果表明,结旁区域的结构对于钠激活和失活至关重要。膜电位和静态电流 - 电压行为可归因于轴突膜。提出了一个关于钠激活 - 失活过程机制的新假说。