Imamoto K
Arch Histol Jpn. 1982 Jul;45(3):275-84.
In rats treated with 6-OHDA in early postnatal days, myelin degeneration was observed in large and medium-sized myelinated nerve fibers belonging to the mesencephalic tract of the trigeminal nerve. Splitting of myelin lamination at the intraperiodic line and irregular excess scrolls were frequent in these fibers, whereas the smaller sized fibers remained intact. Occasionally, naked axons with numerous neurofilaments and neurotubules appeared near the empty myelin scrolls, indicating autolysis of the once-formed myelin sheaths. Some sheaths showed decompaction through loose lamination around the axons. The perikarya of the mesencephalic neurons showed no visible damage, but dark terminals making axo-somatic synapses in the motor nucleus were regarded as degenerating features of the axon-collaterals of the mesencephalic neurons. Thus, the myelin abnormalities were partially attributed to a kind of Wallerian degeneration. A survey of the glial cells in the corpus callosum indicated no remarkable changes in the ratio of the various glial types and in the myelin structures in comparison with those of the controls, although insufficient maturation of oligodendrocytes resulted in a 5-day delay in the onset of myelinogenesis. These findings suggest that the myelin degeneration in the mesencephalic tract is a regionally specific alteration induced by 6-OHDA administrations, probably because of the abnormal accumulation of NA in this area.
在出生后早期用6-羟基多巴胺处理的大鼠中,在属于三叉神经中脑束的大中型有髓神经纤维中观察到髓鞘变性。在这些纤维中,髓鞘板层在周期间线处分裂和不规则的过度卷曲很常见,而较小的纤维保持完整。偶尔,在空的髓鞘卷曲附近会出现带有大量神经丝和神经微管的裸露轴突,表明曾经形成的髓鞘发生了自溶。一些髓鞘通过轴突周围松散的板层显示出结构疏松。中脑神经元的胞体没有可见的损伤,但在运动核中形成轴-体突触的深色终末被认为是中脑神经元轴突侧支的退化特征。因此,髓鞘异常部分归因于一种华勒氏变性。对胼胝体中神经胶质细胞的调查表明,与对照组相比,各种神经胶质类型的比例和髓鞘结构没有明显变化,尽管少突胶质细胞成熟不足导致髓鞘形成起始延迟5天。这些发现表明,中脑束中的髓鞘变性是由6-羟基多巴胺给药引起的区域特异性改变,可能是因为该区域去甲肾上腺素的异常积累。