Miyoshi K, Takauchi S, Hayashi S
Folia Psychiatr Neurol Jpn. 1978;32(2):251-61.
Spongy state and degeneration of the white matter in the 6-aminonicotinamide intoxicated rats were studied neuropathologically and electromicroscopically. Young albino rats, four weeks of age, received 0.1% of 6-aminonicotinamide solution intraperitoneally as a single dose of 10 mg/Kg of body weight. Four hours after the administration, paralysis of the hind limbs occurred in the rats. Neuropathological investigations revealed a characteristic spongy and degenerative change of white matter as well as gray matter of the central nervous system. Corpus callosum, cerebellar cortex, and optic nerves showed edematous and spongy degeneration in the early stage of the experiment. Ultrastructural changes of myelin sheath were initially seen in the vicinity of severely damaged oligodendrocytes. The vacuoles in the myelin, i.e. intramyelinic vacuoles, were formed by splitting between the innermost myelin lamellae and axon. Axons remained usually unchanged in the early stage. The pathogenesis of ultrastructural changes of the white matter in the 6-aminonicotinamide intoxication was discussed.
对6-氨基烟酰胺中毒大鼠的白质海绵状状态和变性进行了神经病理学和电子显微镜研究。四周龄的年轻白化大鼠腹腔注射0.1%的6-氨基烟酰胺溶液，单剂量为10mg/kg体重。给药后四小时，大鼠出现后肢麻痹。神经病理学研究显示中枢神经系统的白质和灰质有特征性的海绵状和变性改变。胼胝体、小脑皮质和视神经在实验早期出现水肿和海绵状变性。髓鞘的超微结构变化最初出现在严重受损的少突胶质细胞附近。髓鞘内的空泡，即髓鞘内空泡，是由最内层髓鞘板层和轴突之间的分裂形成的。轴突在早期通常保持不变。讨论了6-氨基烟酰胺中毒时白质超微结构变化的发病机制。
