Zupan Gordana, Pilipović Kristina, Hrelja Ana, Peternel Sandra
Department of Pharmacology, Faculty of Medicine, University of Rijeka, Braće Branchetta 20, 51 000 Rijeka, Croatia.
Prog Neuropsychopharmacol Biol Psychiatry. 2008 Apr 1;32(3):771-7. doi: 10.1016/j.pnpbp.2007.12.007. Epub 2007 Dec 15.
Electroconvulsive therapy has been used in the treatment of psychiatric disorders since the 1930s, but little progress has been made in understanding the cellular mechanisms underlying its therapeutic and adverse effects. Electroconvulsive shock (ECS) in animals provides a common experimental model for studying the effects of electroconvulsive therapy in humans. In order to examine the changes of the brain oxidative stress parameters in several brain structures in the early time period after ECS-induced seizures, the levels of lipid peroxidation as well as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the rat hippocampus, cerebellum, frontal cortex and the pons/medulla region were determined at different time points during the first 24 h after single ECS-induced seizures. In the hippocampus and cerebellum the levels of lipid peroxidation were unchanged, while the SOD and GSH-Px activities were significantly increased. Levels of lipid peroxidation and the activities of SOD and GSH-Px were not statistically changed in the pons/medulla region. Levels of lipid peroxidation in the frontal cortex were significantly higher in comparison to the control group at all time points examined while the SOD and GSH-Px activities were not statistically changed. In conclusion, the results of the present study indicate that single ECS causes the rat brain structure-specific alterations in the levels of lipid peroxidation as well as in the SOD and GSH-Px activities at different time points within the first 24 h after the seizures induction. Oxidative lipid damage was evident only in the frontal cortex, while the hippocampus, cerebellum and the pons/medulla region remained oxidatively unaffected in our experimental conditions.
自20世纪30年代以来，电休克疗法一直用于治疗精神疾病，但在理解其治疗作用和不良反应背后的细胞机制方面进展甚微。动物电休克（ECS）为研究人类电休克疗法的效果提供了一个常用的实验模型。为了检测ECS诱发癫痫发作后早期几个脑结构中脑氧化应激参数的变化，在单次ECS诱发癫痫发作后的头24小时内，于不同时间点测定大鼠海马体、小脑、额叶皮质以及脑桥/延髓区域的脂质过氧化水平以及超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性。在海马体和小脑中，脂质过氧化水平未发生变化，而SOD和GSH-Px的活性显著增加。脑桥/延髓区域的脂质过氧化水平以及SOD和GSH-Px的活性没有统计学上的变化。在所检测的所有时间点，额叶皮质中的脂质过氧化水平均显著高于对照组，而SOD和GSH-Px的活性没有统计学上的变化。总之，本研究结果表明，单次ECS在癫痫发作诱发后的头24小时内，会在不同时间点导致大鼠脑结构特异性的脂质过氧化水平以及SOD和GSH-Px活性的改变。脂质氧化损伤仅在额叶皮质中明显，而在我们的实验条件下，海马体、小脑和脑桥/延髓区域在氧化方面未受影响。
