Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats  

作　　者：Wan-fu Liu Chao Liu 

机构地区：[1]Department of Anesthesiology, Fuzhou General Hospital of the People's Liberation Army Nanjing Military Region [2]Department of Anesthesiology, Tianjin Chest Hospital

出　　处：《Chinese Medical Sciences Journal》2015年第2期100-107,共8页中国医学科学杂志（英文版）

基　　金：Supported by the National Natural Science Foundation(30972831);the China Postdoctoral Science Foundation(2013M530880)

摘　　要：Objective To explore the possible neurophysiologic mechanisms of propofol and N-methyl-Daspartate(NMDA) receptor antagonist against learning-memory impairment of depressed rats without olfactory bulbs. Methods Models of depressed rats without olfactory bulbs were established. For the factorial design in analysis of variance, two intervention factors were included: electroconvulsive shock groups(with and without a course of electroconvulsive shock) and drug intervention groups [intraperotoneal(ip) injection of saline, NMDA receptor antagonist MK-801 and propofol. A total of 60 adult depressed rats without olfactory bulbs were randomly divided into 6 experimental groups(n=10 per group): ip injection of 5 ml saline; ip injection of 5 ml of 10 mg/kg MK-801; ip injection of 5 ml of 10 mg/kg MK-801 and a course of electroconvulsive shock; ip injection of 5 ml of 200 mg/kg propofol; ip injection of 5 ml of 200 mg/kg propofol and a course of electroconvulsive shock; and ip injection of 5 ml saline and a course of electroconvulsive shock. The learning-memory abilities of the rats was evaluated by the Morris water maze test. The content of glutamic acid in the hippocampus was detected by high-performance liquid chromatography. The expressions of p-AT8Ser202 in the hippocampus were determined by Western blot analysis. Results Propofol, MK-801 or electroconvulsive shock alone induced learning-memory impairment in depressed rats, as proven by extended evasive latency time and shortened space probe time. Glutamic acid content in the hippocampus of depressed rats was significantly up-regulated by electroconvulsive shock and down-regulated by propofol, but MK-801 had no significant effect on glutamic acid content. Levels ofphosphorylated Tau protein p-AT8Ser202 in the hippocampus was up-regulated by electroconvulsive shock but was reduced by propofol and MK-801 alone. Propofol prevented learning-memory impairment and reduced glutamic acid content and p-AT8Ser202 levels induced by electroconvulsive shock. Conclusion ElectroconvulObjective To explore the possible neurophysiologic mechanisms of propofol and N-methyl-Daspartate（NMDA） receptor antagonist against learning-memory impairment of depressed rats withoutolfactory bulbs.Methods Models of depressed rats without olfactory bulbs were established. For the factorialdesign in analysis of variance, two intervention factors were included： electroconvulsive shock groups（with and without a course of electroconvulsive shock） and drug intervention groups [intraperotoneal （ip）injection of saline, NMDA receptor antagonist MK-801 and propofol. A total of 60 adult depressed ratswithout olfactory bulbs were randomly divided into 6 experimental groups （n=10 per group）： ip injectionof 5 ml saline; ip injection of 5 ml of 10 mg/kg MK-801; ip injection of 5 ml of 10 mg/kg MK-801 and acourse of electroconvulsive shock; ip injection of 5 ml of 200 mg/kg propofol; ip injection of 5 ml of 200mg/kg propofol and a course of electroconvulsive shock; and ip injection of 5 ml saline and a course ofelectroconvulsive shock. The learning-memory abilities of the rats was evaluated by the Morris water mazetest. The content of glutamic acid in the hippocampus was detected by high-performance liquidchromatography. The expressions of p-AT8Ser202 in the hippocampus were determined by Western blotanalysis.Results Propofol, MK-801 or electroconvulsive shock alone induced learning-memory impairmentin depressed rats, as proven by extended evasive latency time and shortened space probe time. Glutamic acid content in the hippocampus of depressed rats was significantly up regulated by electroconvulsive shock and down-regulated by propofol, but MK-801 had no significant effect on glutamic acid content. Levels of phosphorylated Tau protein p-AT8Ser202 in the hippocampus was up-regulated by electroconvulsive shock but was reduced by propofol and MK-801 alone. Propofol prevented learning-memory impairment and reduced glutamic acid content and p-AT8Ser202 levels induced by electroconvulsive shock. Conclusion Elec

关 键 词：PROPOFOL Tau protein learning-memory ABILITIES GLUTAMATE electroconvulsive therapy 

分 类 号：R749.4[医药卫生—神经病学与精神病学]