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Published on: May 3, 2017
[Influence of Electroacupuncture Intervention on Glutamic Acid and Ca2+ Contents and Expression of NMDA Receptor
Qian Zhang1, Chuang Zhang2, Jia-Yin Zhang1
1College of Traditional Chinese Medicine, Hebei Medical University, Shijiazhuang 050091, China.
Objective:
To observe the influence of electroacupuncture (EA) intervention on hippocampal glutamate (Glu) and Ca2+ contents, and expression of Glu-N-methyl-D-aspartic acid receptor(NMDAR) and the learning-memory ability in vascular dementia (VD) rats, so as to reveal its mechanisms underlying improvement of VD.
Methods:
SD rats were rando-mized into sham operation (sham) group (n=9), model group (n=11) and EA groups (n=10). The VD model was established by repeated bilateral common carotid arteries occlusion and reperfusion plus intraperitoneal injection of sodium nitroprusside. EA (2 Hz, 2 mA) was applied to "Baihui" (GV 20)-"Housanli" (ST 36) and "Geshu" (BL 17)-"Dazhui" (GV 14) for 10 min, once a day for 15 consecutive days. The neurological function was assessed by using stroke index (0-10 points) and neurological deficit scaling(0-10 points). The learning-memory ability was evaluated by using step-down tests. The contents of Glu and Ca2+ in the right hippocampal tissue were determined by using aspectrophotometer and the expression of NMDAR protein in the right hippocampus was detected by immunoblotting.
Results:
Compared with the sham group, the stroke index and neurological deficit scores, and the reaction latency and the error times of step-down tests, as well as the contents of Glu and Ca2+ and the expression level of NMDAR in the right hippocampus were significantly increased in the model group (P<0.05, P<0.01), while the step-through latency was considerably decreased (P<0.01), suggesting a neurological disorder and a cognitive decline. After EA intervention, the reaction latency and error times of step-down tests, the contents of Glu and Ca2+ and the expression level of NMDAR in the right hippocampus were significantly down-regulated, and the step-through latency was notably increased in comparison with the model group (P<0.01).
Conclusions:
EA intervention is able to improve the cognitive ability of VD rats, which may be associated with its effects in reducing the excitatory neurotoxicity of hippocampal Glu-NMDAR and lowering cellular Ca2+ load to resist neuronal injury.
