摘要
本研究通过在饲料中掺入cuprizone饲育小鼠,建立髓鞘可再生的急性脱髓动物模型,并利用髓鞘染色和原位杂交后免疫组化双标技术,检测髓鞘脱失和再生状况以及少突胶质前体细胞的改变。结果表明,给予cuprizone6周后,动物胼胝体严重脱髓鞘,少突胶质前体细胞在髓鞘脱失区域集聚,且增殖活跃;恢复正常饲料饲养4周后,髓鞘基本恢复正常形态。由此推测,在cuprizone介导的急性脱髓动物模型髓鞘脱失和再生过程中,少突胶质前体细胞的增殖活化为髓鞘再生提供了基础。
Cuprizone diet C57BL/6 mice were used to establish acutely demyelinated model in the present study. In these mice, status of demyelination and remyelination were studied by using myelin staining, and the changes of oligedendrocyte progenitors (OLPs) were demonstrated by immunohistochemistrical staining following in situ hybridization. The results showed that obvious demyelination and proliferation of OLPs occurred in corpus callosum following 6 weeks of exposure to cuprizone, and myelin became normal by remyelination after the mice were returned to 4 weeks of normal diet. It suggests that proliferation of OLPs is contributed to remyelination in cuprizone induced acutely demyelinated animal model.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2007年第2期191-194,共4页
Chinese Journal of Neuroanatomy
基金
辽宁省科技厅博士启动基金(No.20051071)资助项目