论文部分内容阅读
目的:研究EGB761改善东莨菪碱致小鼠记忆障碍的突触机制。方法:腹腔注射EGB761连续7d。采用东莨菪碱造成小鼠记忆障碍模型,分别用Y型迷宫测试小鼠进行自发交替和活动能力,离体脑片细胞外记录技术观测海马长时程增强(LTP)的变化。结果:与模型组比较,EGB761可使小鼠的自发交替的百分率明显增高,活动能力明显下降,LTP诱发成功率和群峰电位(PS)振幅增大率明显增高。结论:EGB761可明显增强突触传递效能,改善东莨菪碱东造成小鼠记忆障碍。
Objective: To study the mechanism of EGB761 in improving the synaptic mechanism of scopolamine-induced memory impairment in mice. METHODS: Intraperitoneal injection of EGB761 was continued for 7 days. The scopolamine was used to model mice with memory impairment. The mice were tested with Y-maze to perform spontaneous alternation and activity. The extracellular recordings of isolated brain slices were used to observe the changes of long-term potentiation (LTP) in the hippocampus. RESULTS: Compared with the model group, EGB761 significantly increased the percentage of spontaneous alternation in mice, and the activity was significantly decreased. The LTP-induced success rate and group peak potential (PS) amplitude increased significantly. Conclusion: EGB761 can significantly enhance the efficiency of synaptic transmission and improve memory impairment of mice caused by scopolamine.