Effects of electroacupuncture on learning and memory in experimental Alzeheimer′s disease
10.3760/cma.j.issn.0254-1424.2016.05.005
- VernacularTitle:电针对阿尔茨海默病模型大鼠学习记忆能力及海马NSF表达的影响
- Author:
Xiaoyan SHEN
;
Ruolan LIU
;
Chen SHEN
;
Jun TIAN
- Publication Type:Journal Article
- Keywords:
Alzheimer′s disease;
Electroacupuncture;
Hippocampus;
N-ethylmaleimide-sensitive fu-sion factor;
AMPA-receptor
- From:
Chinese Journal of Physical Medicine and Rehabilitation
2016;38(5):340-343
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of electroacupuncture ( EA) on learning and memory ability and the expression of N-ethylmaleimide-sensitive fusion factor ( NSF) in experimental Alzheimer′s disease ( AD) and to explore the mechanism involved. Methods Sixty healthy, male Sprague-Dawley rats were randomly divided into a normal group, a sham operation group, a model group and an EA group, each of 15.The model group and the EA group were injected with Aβ25-35 bilaterally in the CA1 area of the hippocampus, while the sham operation group was injected with the same amount of normal saline in the same regions. From the 1stday after the AD model had been es-tablished successfully, EA was applied to the Shen Shu ( BL23) and Bai Hui ( GV20) acupoints in the EA group once a day,6 days a week for 2 weeks. No EA was given to the other 3 groups. After the treatment, Morris water maze tests were conducted to determine assess the rats′ learning and memory ability, and immunohistochemical methods were used to test the expression level of NSF in the CA1 areas of the rats′hippocampus. Results The average es-cape latent period of the EA group was significantly shorter than that of the model group and their average platform crossing time was significantly longer. The average expression of NSF in the EA group measured as integrated optical intensity was significantly higher than that in the model group. Conclusion EA can effectively improve learning and memory ability in AD, at least in rats. The mechanism may involve increasing the expression of NSF in the CA1 area of the hippocampus.
