Allt G
J Neurocytol. 1975 Feb;4(1):63-76. doi: 10.1007/BF01099096.
Pathological breakdown of the node of Ranvier in experimental allergic neuritis (EAN) in the rabbit was examined by electron microscopy. The study was concerned principally with the mechanism of disruption of paranodal myelin. Two types of change in myelin structure were observed, both apparently related to the presence of cytoplasmic processes of macrophages: (1) a vesicular disorganization of myelin lamellae and (2) a separation of myelin lamellae. Both methods of disorganization were used by macrophages as they apparently lifted off the myelin terminal loops of the paranode from the underlying axon and also penetrated between myelin loops and adjoining myelin lamellae. In some pathologically damaged nodes of Ranvier no macrophages were observed. The findings raise important immunological and electrophysiological questions concerning the involvement of the macrophage in the autoimmune response and the effect of the loss of paranodal myelin on nerve conduction.
通过电子显微镜检查了兔实验性变应性神经炎(EAN)中朗飞结的病理破坏情况。该研究主要关注结旁髓鞘破坏的机制。观察到髓鞘结构的两种变化,这两种变化显然都与巨噬细胞的胞质突起有关:(1)髓鞘板层的小泡状紊乱;(2)髓鞘板层的分离。巨噬细胞采用这两种紊乱方式,显然是将结旁的髓鞘终末环从下方的轴突上掀起,并且还穿透髓鞘环与相邻的髓鞘板层之间。在一些病理受损的朗飞结中未观察到巨噬细胞。这些发现提出了关于巨噬细胞参与自身免疫反应以及结旁髓鞘丧失对神经传导的影响的重要免疫学和电生理学问题。