Saida K, Saida T, Kayama H, Nishitani H
Ann Neurol. 1984 Jun;15(6):581-9. doi: 10.1002/ana.410150611.
Alterations of nodal and paranodal axolemma of the rat sciatic nerve were investigated in antigalactocerebroside serum-induced demyelination. A ferric ion-ferrocyanide (FeFCN) stain that appears to stain the regions with a high sodium channel density in nerve fibers was applied. When acute conduction block was initiated 20 to 180 minutes after the antiserum injection, myelin terminal loops began to be detached from the paranodal axolemma and reaction product of FeFCN stain originally localized at the nodes decreased in density and extended to the paranodal axolemma. By the time that complete conduction block was established, 5 hours after the injection, FeFCN stain was barely detectable around the nodal area. The loss of staining was associated with detachment and vesiculovacuolar degeneration of the paranodal myelin. This rapid deterioration and disappearance of normal cytochemical characteristics of the axolemma in the presence of only modest paranodal demyelination could be a morphological correlate of the loss of excitability of the axon membrane.
在抗半乳糖脑苷脂血清诱导的脱髓鞘过程中，研究了大鼠坐骨神经结旁和结间轴膜的改变。应用了一种铁离子-亚铁氰化物（FeFCN）染色法，该方法似乎能对神经纤维中钠通道密度高的区域进行染色。在注射抗血清后20至180分钟开始出现急性传导阻滞时，髓鞘终末环开始从结旁轴膜分离，原本位于结处的FeFCN染色反应产物密度降低并扩展到结旁轴膜。到注射后5小时完全传导阻滞形成时，结区周围几乎检测不到FeFCN染色。染色的丧失与结旁髓鞘的分离和小泡空泡变性有关。在仅存在适度结旁脱髓鞘的情况下，轴膜正常细胞化学特征的这种快速恶化和消失可能是轴突膜兴奋性丧失的形态学相关因素。
