Effects of propofol on CaMK Ⅱ α activity in hippocampus in mentally depressed rats after electroconvulsive therapy / 中华麻醉学杂志

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.