目的：研究电针是否通过调节老年性痴呆模型小鼠海马N -甲基- D -天冬氨酸型谷氨酸受体(NMDARs)的表达，保护认知能力，探讨电针防治老年性痴呆的作用机制。方法：6月龄雄性APPswe/PS1 dE9 (APP/PS1)双转基因小鼠作为老年性痴呆动物模型，随机分为痴呆模型组及电针治疗组，以同月龄C57BL/6野生型小鼠为对照组。选用百会穴、印堂穴及水沟穴，电针治疗20min/次，隔日干预1次。治疗14次后，运用Morris水迷宫测试观察电针治疗对实验小鼠认知能力的影响，以Western Blot方法检测小鼠海马NMDARs表达水平的变化。结果：痴呆模型组小鼠逃避潜伏期比对照组增加，第Ⅲ象限平台穿越次数及停留时间均减少；海马NMDAR1及NMDAR2B的蛋白表达水平下降。与痴呆模型组比较，电针治疗组逃避潜伏期明显减少；NMDAR1及NMDAR2B的表达增加。结论：电针可改善老年性痴呆模型小鼠学习记忆能力，其机制可能与增加海马NMDARs表达有关。
Objective：To observe whether expression of NMDARs in hippocampus can be adjusted by electroacupuncture (EA) to enhance the cognition of Alzheimer's disease(AD) mice，and to explore the mechanism of the EA therapy for AD. Methods：Sixteen 6-month-old APPswe/PS1 dE9 (APP/PS1) transgenic mice were randomly divided into AD model group and EA treatment group，with eight C57BL/6J wild type mice as the normal control group. Baihui (GV20), Yintang (GV29) and Shuigou(GV26) were applied，EA treatment for 20 min every other day. After 4 weeks，Morris water maze test was used to evaluate the learning and memory ability of mice，and western blot was used to detect the expression level of NMDARs in the hippocampus of mice. Results： the escape latency in the AD model group was significantly higher than that in the normal control group，while platform crossover number and the percentage of duration in the Ⅲ quadrant of AD model group were significantly reduced; the expressions of NMDAR1 and NMDAR2B in the hippocampus were significantly decreased. Compared with AD model group，the escape latency in EA treatment group was significantly decreased，the levels of NMDAR1 and NMDAR2B in the hippocampus were significantly increased. Conclusion：EA therapy can improve the cognition of the AD mice. The mechanism may be related to the increased expression of NMDARs in hippocampus.