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作 者:唐玉红[1] 谢扬高[1] 柴慧霞[1] 肖邦良[2] 王远萍[3]
机构地区:[1]华西医大学生理学教研室 [2]华西医大学毒理学教研室 [3]华西医大学电子显微镜室
出 处:《华西医科大学学报》1991年第1期39-42,共4页Journal of West China University of Medical Sciences
基 金:国家自然科学基金
摘 要:作者用酶组化方法观察大鼠马桑内酯(CL)腹腔点燃各阶段大脑皮质、海马及小脑乙酰胆碱酯酶、辅酶I黄递酶、细胞色素氧化酶、乳酸脱氢酶、琥珀酸脱氢酶、酸性非特异性酯酶、酸性磷酸酶及碱性磷酸酶等8种酶活性变化,结果提示:CL引起点燃发作机理可能与其抑制脑内乙酰胆碱酯酶活性有关。电镜观察发现点燃大鼠的海马神经元有变性改变,该损伤可能是由CL毒性所致。Kindling model of epilepsyinduced by intraperitoneal injection ofCoriaria lactone (CL) was used in the ex-periment. The dose of CL was 1. 25mg/kg.Thirty rats in various periods of kindlingwere killed and the materials of cerebralcortex,hippocampus and cerebellum weredrawn. The enzyme activities of AchE,NADHD, CCO, LDH, SDH, AcP, ANAE and AkP of these areas were observedwith enzymohistochemical techniques. In another three kindled rats, two blankcontrol rats and two NS conirol rats,the ultrastructure of neurons in hippocam- pus were obseved. The results of experiments showed anincreased activity of enzymes related tosaccharometabolism and energy matabolism,indicating that the metabolism of brain inrats was increased by repeated kindlingseizures. The mechanism of kindling seizureinduced by CL may be related to inhibitoryeffect of CL on AchE activity of brain. Thedegeneration damage of brain neurons inkindled rats may result from using CL fora long time.
分 类 号:R742.102[医药卫生—神经病学与精神病学]
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