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2,6-二异丙基苯酚与NMDAR阻滞剂逆转嗅球切除抑郁模型大鼠电休克后空间学习记忆障碍的神经心理学机制之比较
Comparison of the neuropsychology mechanisms of 2,6-Diisopropylphenol and NMDA receptor antagonist protects against the impairment of learning-memory induced by electroconvulsive shock in depressed ra

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DOI:
作者:
刘超，闵苏，魏珂，刘东，董军，罗洁，刘小滨
LIU C, MIN S, WEI K, LIU D, DONG J, LUO J, LIU XB
作者单位:
重庆医科大学附属第一医院麻醉科
Department of Anesthesiology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University
关键词:
2,6-二异丙基苯酚，电休克，学习记忆，τ蛋白
2,6-Diisopropylphenol; Electroconvulsive therapy; Learning and memory; Tau protein
摘要:
目的：比较2,6-二异丙基苯酚和NMDAR阻滞剂对ECT后抑郁大鼠学习记忆的影响和作用机制的异同。方法：设2组干预因素，即ECT干预（两水平：无处置、施行一个疗程ECT）和药物干预（三水平：腹腔注射生理盐水、2,6-二异丙基苯酚、NMDAR阻滞剂MK-801）的所有组合（2×3析因设计）。ECT后进行Morris水迷宫检测，高效液相色谱法检测Glu在海马中的表达，免疫组织化学SP法和免疫印迹法检测p-AT8Ser202和GSK-3β1H8在海马中的表达。结果：2,6-二异丙基苯酚、NMDAR阻滞剂及ECT均可造成大鼠学习记忆障碍。ECT可明显增加海马中Glu的浓度；2,6-二异丙基苯酚可降低海马中Glu的浓度；而NMDAR阻滞剂对海马中Glu的浓度无明显影响。ECT可增加海马中磷酸化Tau蛋白p-AT8Ser202及促进其磷酸化的GSK-3β1H8蛋白的表达；2,6-二异丙基苯酚和NMDAR阻滞剂可减缓海马中磷酸化Tau蛋白p-AT8Ser202及促进其磷酸化的p-AT8Ser202蛋白的表达上调。结论：2,6-二异丙基苯酚则可通过降低海马Glu浓度减缓Tau蛋白的磷酸化程度改善ECT后认知障碍。
Objective This study explore the reversion of 2,6-Diisopropylphenol and MK801 against the impairment of learning-memory and the hyperphosphorylation of tau protein induced by ECT in depressed rats. Methods As the analysis of variance of factorial design set up two intervention factors which are ECT groups (two levels: no disposition; ECT) and the drug intervention groups (three level: iv Saline; iv MK-801; iv 2,6-Diisopropylphenol). Forty-eight adult depression model rats whose olfactory bulbs were removed were randomly divided into six experimental groups (n=8, in each group): (I) 5ml Saline was injected peritoneally in the depression model rats; (II) 5ml MK-801 was injected peritoneally in the depression model rats by dosage of 10mg/kg; (III) 5ml MK-801 was injected peritoneally in the depression model rats and giving ECT by dosage of 10mg/kg; (IV) 5ml 2,6-Diisopropylphenol was injected peritoneally in the depression model rats by dosage of 200mg/kg; (V) 5ml 2,6-Diisopropylphenol was injected peritoneally in depression model rats by dosage of 200mg/kg and giving ECT; (VI) 5ml Saline was injected peritoneally in the depression model rats and giving ECT. The morris water maze test were started. Detect of the content of glutamate in the hippocampus of rats by HPLC. Detect of the expression of Tau protein which includes p-AT8Ser202 and GSK-3β1H8 in the hippocampus of rats with the methods of IHC-SP and WB. Results 2,6-Diisopropylphenol and MK801 and ECT can induce the impairment of learning-memory in depressed rats. ECT can significantly up-regulated the content of glutamate, which was not affected by MK801, in the hippocampus of depressed rats which was reduces by the 2,6-Diisopropylphenol. ECT and the drugs does not affect the total Tau protein in the hippocampus of rats. ECT can up-regulated the hyperphosphorylation of tau protein in the hippocampus of rats which is can be reduced by 2,6-Diisopropylphenol and MK801. Conclusion 2,6-Diisopropylphenol protects against the impairment of learning-memory and reduce the hyperphosphorylation of tau protein induced by electroconvulsive shock in depressed rats.

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