These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: [Influence of Electroacupuncture Intervention on Glutamic Acid and Ca2+ Contents and Expression of NMDA Receptor Protein in Hippocampus in Vascular Dementia Rats]. Author: Zhang Q, Zhang C, Zhang JY, Zhang HZ, Li XF, Xiao HL, Sun YH, Xing HJ, Xu XK, Liang YL, Zhang X, Zhang XQ, Li AY. Journal: Zhen Ci Yan Jiu; 2016 Dec 25; 41(6):509-14. PubMed ID: 29071893. Abstract: 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.[Abstract] [Full Text] [Related] [New Search]