Del Bigio M R, Zhang Y W
Department of Pathology, University of Manitoba, Winnipeg, Canada.
Exp Neurol. 1998 Nov;154(1):157-69. doi: 10.1006/exnr.1998.6922.
We hypothesized that hydrocephalus can cause death of brain cells and that generation of new brain cells might compensate for the cell loss. Hydrocephalus was induced in 3-week-old rats by injection of kaolin into the cisterna magna. The brains were studied 1 to 4 weeks later by histochemical, immunochemical, and ultrastructural methods. The ventricles enlarged progressively. Some axons in the corpus callosum were injured as early as 1 week, but axonal damage was not prevalent until 4 weeks when ventriculomegaly became severe. Dying cells detected by DNA end labeling and often identified as oligodendrocytes by electron microscopy were evident in white matter. Late-stage hydrocephalus was associated with a significant increase in the quantity of dying cells. Hydrocephalus was associated with increased Ki67 labeling and bromodeoxyuridine incorporation in the subependymal zone. Reactive changes were identified among astrocytes, oligodendroglia, and microglia. We conclude that hydrocephalus causes, in addition to axonal injury, gradual cell death in the cerebrum, particularly the white matter. The brain response includes production of new glial cells, but whether the new cells play any beneficial role remains unknown.
我们推测脑积水可导致脑细胞死亡，而新生脑细胞的产生可能会弥补细胞损失。通过向3周龄大鼠的大池内注射高岭土来诱导脑积水。1至4周后，采用组织化学、免疫化学和超微结构方法对大脑进行研究。脑室逐渐扩大。早在1周时，胼胝体中的一些轴突就受到损伤，但直到4周脑室扩大变得严重时，轴突损伤才普遍出现。通过DNA末端标记检测到的死亡细胞，经电子显微镜观察常被鉴定为少突胶质细胞，在白质中很明显。晚期脑积水与死亡细胞数量的显著增加有关。脑积水与室管膜下区Ki67标记和溴脱氧尿苷掺入增加有关。在星形胶质细胞、少突胶质细胞和小胶质细胞中发现了反应性变化。我们得出结论，脑积水除了导致轴突损伤外，还会导致大脑尤其是白质中的细胞逐渐死亡。大脑的反应包括产生新的胶质细胞，但新细胞是否发挥任何有益作用尚不清楚。
