摘要
目的 :研究D 半乳糖合并Meynert基底核损毁Alzheimer病 (AD)大鼠模型海马突触可塑性的变化。方法 :通过0 .96 %D 半乳糖致亚急性损伤及鹅膏蕈氨酸损毁Meynert基底核建立AD动物模型 ,应用行为学测试、电生理学方法和电镜观察 ,研究AD模型大鼠海马突触形态结构和长时程增强现象 (long termpotentiation ,LTP)的变化。结果 :①AD模型大鼠在Morris水迷宫的学习记忆能力明显低于对照组 ;②AD大鼠海马CA1区突触的数密度、面密度明显减少 ;③AD模型大鼠海马齿状回产生的LTP较对照组明显降低。结论
Ami: To study the changes of synaptic plasticity in rat model with Alzheimer disease ( AD ). Methods: AD rat model was conducted by D-galactose intraperitoneal injection combined with lesions of nucleus basalis of Meynert ( nbM ). Behavioral performance, LTP in dentate gyrus and synaptic morphology in hippocampal CA1 were observed. Results:① Escape latencies in place test in model rats were longer than that in control rats, and swimming time and distance between the two groups in platform quadrant were significant differently (P<0.01). ② The numerical density (Nu) and surface density (Su) of synaptic contact zones markedly decreased (P<0.01) in model rats. ③ Augment of population spike ( PS ) in perforant path-dentate gyrus of model rats after high frequency stimulation was smaller than that of the control (P<0.05). Conclusion: The results suggest that the decreased synaptic plasticity in hippocampus could responsible for the impairment of spatial learning of model rats.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2002年第1期18-22,共5页
Chinese Journal of Applied Physiology
基金
国家"九五"重点攻关项目 ( 96 90 6 0 9 0 2 )
国家医药技术创新博士项目 ( 96 90 1 0 6 46 )
