Department of Neuropathology, Institute of Psychiatry and Neurology, Warsaw, Poland.
Folia Neuropathol. 2012;50(4):397-406. doi: 10.5114/fn.2012.32374.
Maternal ethanol consumption during pregnancy may cause foetal alcohol syndrome (FAS). Our experiments of ethanol-treated female rats were based on the FAS model in humans; therefore, the results obtained may help explain the clinical mechanism of the disease development. The ultrastructural examination of the cerebellar cortex of ten-day-old rat pups of ethanol-treated dams during pregnancy (group IA), pregnancy and lactation (group IIA), and lactation (group IIIA) revealed that alcohol administration leads to a delayed maturation of Purkinje cells. This was most strongly manifested in the pups of dams treated with ethanol during pregnancy and lactation. Moreover, this study showed degenerative changes in Purkinje cells as well as in granular layer cells in all experimental groups. There was a difference in the ultrastructural picture of both types of dying cells, which might result from different time frame of their sensitivity to ethanol administration. The quantitative analysis showed the most pronounced decrease in the density of Purkinje cells in the posterior superior fissure of cerebellar cortex in the pups of dams treated with ethanol during pregnancy.
母亲在怀孕期间饮酒可能会导致胎儿酒精综合征(FAS)。我们对雌性大鼠进行乙醇处理的实验是基于人类的 FAS 模型;因此,获得的结果可能有助于解释疾病发展的临床机制。对怀孕(IA 组)、怀孕和哺乳期(IIA 组)以及哺乳期(III 组)期间接受乙醇处理的母鼠的 10 天大的幼鼠小脑皮质的超微结构检查显示,酒精摄入会导致浦肯野细胞成熟延迟。在接受怀孕和哺乳期乙醇处理的母鼠的幼鼠中,这种情况表现得最为强烈。此外,这项研究显示所有实验组的浦肯野细胞和颗粒层细胞都发生了退行性变化。两种死亡细胞的超微结构图像存在差异,这可能是由于它们对乙醇处理的敏感性的时间框架不同所致。定量分析显示,在接受乙醇处理的母鼠的幼鼠中,小脑皮质后上裂的浦肯野细胞密度下降最为明显。