神经调节蛋白1及其受体ErbB4在精神分裂症小鼠前额叶皮质中的表达变化

目的:探讨精神分裂症神经调节蛋白1(NRG-1)及其受体(ErbB4)与少突胶质细胞脱髓鞘和髓鞘再生之间的关系.方法:采用双环己酮草酰二腙(CPZ)诱导的少突胶质细胞脱髓鞘制备精神分裂症小鼠动物模型.动物分为6组,对照组(食物中未添加CPZ),CPZ喂养2周、3周、4周组,第4周后停止给予CPZ,继续正常喂养1周即5周组;停止给予CPZ后,继续正常喂养2周即6周组.通过实时定量PCR及免疫印迹检测,观察NRG-1和ErbB4在小鼠大脑额叶脱髓鞘和髓鞘再生过程中的表达变化.结果:NRG-1 mRNA和蛋白的表达在第2周、第3周和第4周CPZ组较对照组、第5周和第6周明显降低.ErbB4 mRNA和蛋白的表达在各组与对照组比较均增强.ErbB4在第5周和第6周mRNA和蛋白的表达明显高于第2周、第3周和第4周CPZ组.结论:在小鼠精神分裂症形成过程中,NRG-1和ErbB4的表达变化与少突胶质细胞的脱髓鞘和髓鞘再生有关系.

Expression of neuregulin-1 and ErbB4 receptor in the prefrontal cortex of schizophrenic mouse model

Objective :To explore the relationship between expression of neuregulin-1/ErbB4 receptor and demyelination/remyelination of oligodendrocytes in the schizophrenic mouse model. Methods :Schizophrenic model was established via cuprizone-induced demyelination of oligodendrocytes in mice. Animals were divided into six groups. Group week 1 was control with no cuprizone in food. Group week 2 was fed with cuprizone for two weeks. Group week 3 was fed with cuprizone for three weeks. Group week 4 was fed with cuprizone for four weeks. In group week 5,the cuprizone feeding was stopped after week 4 and then continued with normal feeding for one week. In group week 6,the cuprizone feeding was ended after week 4 and then continued with normal feeding for two weeks. Quantitative real-time PCR and Western blotting were used to detect the NRG-1 and ErbB4 receptor expression in the demyelination and remyelination in the prefrontal cortex of rats. Results :The results showed that the expression of NRG-1 mRNA and protein in the group week 2,group week 3 and group week 4 significantly decreased compared with the control,group week 5 and group week 6. The expression of ErbB4 mRNA and protein increased in each group compared with the control,and the expression of ErbB4 mRNA and protein in group week 5 and group week 6 increased significantly compared with that of group week 2 and group week 3 and group week 4. Conclusion :Our findings suggest that NRG1/ErbB4 is closely related to demyelination and remyelination of oligodendrocytes in the development of schizophrenia..