Effects of propofol on CaMK Ⅱ α activity in hippocampus in mentally depressed rats after electroconvulsive therapy
10.3760/cma.j.issn.0254-1416.2011.11.004
- VernacularTitle:异丙酚对抑郁大鼠电休克处理后海马CaMKⅡα活性的影响
- Author:
Xiao LI
;
Su MIN
;
Wei LI
;
Jie LUO
;
Ke WEI
;
Ping LI
;
Xiaobin LIU
;
Xinzhu QI
- Publication Type:Journal Article
- Keywords:
Propofol;
Electroconvulsive therapy;
Depression;
Calcium-calcium-calmodulin-dependent protein kinase type 2;
Hippocampus
- From:
Chinese Journal of Anesthesiology
2011;31(11):1302-1305
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effects of propofol on calcium/calmodulin-dependent protein kinase Ⅱ α ( CaMK Ⅱ α) activity in hippocampus in mentally depressed rats after electroconvulsive therapy (ECT).MethodsHealthy adult male SD rats aged 2-3 months weighing 180-220 g were used in this study.Mentally depressed model was induced by chronic unpredictable mild stress.Forty mentally depressed rats were randomly divided into 4 groups (n =10 each): mental depression group (group D),propofol group (group P),ECT group (group E),propofol + ECT group (group DPE).Groups D and P received intraperitoneal normal saline 8 ml/kg or propofol 80 mg/kg once a day for 7 consecutive days respectively.Group E received ECT once a day for 7 consecutive days.Group DPE received propofol 80 mg/kg + ECT once a day for 7 consecutive days.Sucrose preference test was performed at 1 d before and 1 d after treatment,and Morris water maze test was performed at 1 d before and 3 d after treatment.The rats were sacrificed after Morris water maze test,and hippocampi were removed for determination of CaMK Ⅱ α and phosphorylated CaMK Ⅱ α(pCaMK Ⅱ α )expression,and pCaMK Ⅱ α/CaMK Ⅱ α ratio was caculated.ResultsCompared with group D,the sucrose preference percentage was significantly increased in groups E and DPE,the escape latency prolonged and space exploration time shortened,and the expression of CaMK Ⅱ α and pCaMK Ⅱ α down-regulated,pCaMK Ⅱ α/CaMK Ⅱ α ratio decreased in group E,the escape latency was significantly shortened and space exploration time prolonged,and the expression of pCaMK Ⅱ α up-regulated in group DPE ( P ＜ 0.05).Compared with group E,the escape latency was significantly shortened,space exploration time prolonged,and the expression of CaMK Ⅱ α and pCaMK Ⅱ α up-regulated,and pCaMK Ⅱ α/CaMK Ⅱ α ratio increased in group DPE ( P ＜ 0.05).ConclusionPropofol can reduce the cognition impairment induced by ECT in mentally depressed rats through enhancing CaMK Ⅱ α activity in hippocampus.
