The effects of electroacupuncture on the expression and phosphorylation of AMPAR and CaMK Ⅱ in hippocampus in rats with vascular dementia
10.3760/cma.j.issn.0254-1424.2014.09.001
- VernacularTitle:电针对血管性痴呆大鼠海马组织GluA1和CaMKⅡ表达及其磷酸化的影响
- Author:
Huiying LIANG
;
Yangyang LIN
;
Tiebin YAN
;
Lin LIAO
;
Juntao DONG
- Publication Type:Journal Article
- Keywords:
Electroacupuncture;
Dementia,vascular;
Memory;
Hippocampus;
Gene expression
- From:
Chinese Journal of Physical Medicine and Rehabilitation
2014;36(9):657-661
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of electroacupuncture(EA) on the hippocampal expression of GluA1,pGluA1,CaMK Ⅱ and pCaMK Ⅱ in rats with vascular dementia(VD),so as to find out the underlying mo lecular mechanisms of EA in treating VD.Methods Thirty-two Wistar rats were randomly divided into a shamoperation group,a model group,a sham-acupuncture group,and an EA group (8 in each group).Permanent bilateral common carotid artery occlusion was performed to model vascular dementia in the model group,the shamacupuncture group and the EA group,while exposure but no occlusion of the bilateral common carotid were performed in the sham-operating group.Novel object recognition test was adopted to prove the establishment of VD rat model.All the rats were kept in an immobilization apparatus while receiving treatments.EA was applied ontoBaihui (GV20) and Zusanli (ST36) in EA group for 30 min,once daily for 7 days.Sham-acupuncture group were treated with needles inserted 0.5 mm superficially.And the sham-operation group and the model group were only immobilized.The protein expression of GluA1,pGluA1,CaMK Ⅱ and pCaMK Ⅱ in hippocampal tissue was detected by western blotting.Results The expression of GluA1 in the model group (1.216 ± 0.102) was significantly less than in the sham-operating group (1.918 ± 0.137) (P ＜ 0.05).The expression of GluA1 in the EA group (1.653 ± 0.169) was significantly higher than in the model group (1.216 ± 0.102) and in sham-acupuncture group (1.231 ±0.188) (P＜0.05).The expression of CaMKⅡ in the model group (1.516±0.392) was less than in the sham-operating group (2.187 ± 0.231) (P ＜ 0.05).The expression of CaMK Ⅱ in the EA group (2.733 ±0.387) was significantly higher than in the model group (1.516 ±0.392) and sham-acupuncture group (1.493 ±0.205) (P＜0.05).The expression ofpGluA1 in the model group (1.502 ±0.419) was less than in the sham-operating group (2.253 ± 0.244) (P ＜ 0.05).The expression of pGluA1 in the EA group (2.382 ± 0.308) was significantly higher than in the model group (1.502 ± 0.419) and the sham-acupuncture group (1.498 ± 0.223) (P ＜ 0.05).The expression of pCaMK Ⅱ in the model group (0.394 ± 0.227) was less than in the sham-operating group (0.667 ±0.175) (P＜0.05).The expression ofpCaMKⅡ in the EA group (1.189± 0.346) was significantly higher than in the model group (0.394 ± 0.227) and the sham-acupuncture group (0.408 ± 0.231) (P ＜ 0.05).Conclusion EA can enhance the protein expression and phosporylation of GluA1 and CaMK Ⅱ,causing silent synapses transforming into functional synapses,and consequently,long term potentiation was facilitated and cognitive impairment was improved by EA.
