Abstract
Objective To evaluate the effects of propofol on neuronal nitric oxide synthase (nNOS) activity and carboxy-terminal PDZ ligand of nNOS (CAPON) expression in hippocampal neurons after electroconvulsive therapy (ECT) in mentally depressed rats.Methods Healthy adult male Sprague-Dawley rats,aged 2-3 months,weighing 200-250 g,were used in this study.Mentally depression was induced by exposing the rats to chronic unpredictable mild stress (CUMS).Forty mentally depressed rats were randomly divided into 4 groups (n =10 each):mental depression group (group D),propofol group (group DP),ECT group (group DE),and propofol +ECT group (DPE group).Groups D and DE received intraperitoneal normal saline 8 ml/kg,and in addition group DE received ECT once a day for 7 consecutive days.Groups DP and DPE received intraperitoneal propofol 80 mg/kg,and in addition after the righting reflex disappeared,group DPE received ECT once a day for 7 consecutive days.All rats underwent sucrose preference test and Morris water maze test before CUMS,after CUMS,and after the end of treatment.The rats were sacrificed after completion of Morris water maze test and hippocampi were removed for determination of nNOS and CAPON expression in hippocampal neurons.Results Compared with group D,the sucrose preference percentage was significantly increased in DE and DPE groups,the escape latency was prolonged and space exploration time was shortened,the expression of nNOS in hippocampal DG,CA1 and CA3 regions was up-regulated and the expression of CAPON in hippocampal DG,CA1 and CA3 regions was down-regulated in group DE,and the expression of nNOS and CAPON in hippocampal DG,CA1 and CA3 regions was downregulated in group DP (P ＜ 0.05).Compared with group DE,the escape latency was significantly shortened and space exploration time was prolonged,the expression of nNOS in hippocampal DG,CA1 and CA3 regions was down-regulated and the expression of CAPON in hippocampal DG,CA1 and CA3 regions was up-regulated in group DPE (P ＜ 0.05).Conclusion The mechanism by which propofol reduces the cognitive impairment induced by ECT in mentally depressed rats is related to inhibition of nNOS activity and up-regulation of CAPON expression in hippocampal neurons. Key words: Propofol; Electroconvulsive therapy; Depression; Nitric oxide synthase type Ⅰ ; Hippocampus
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