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首页> 外文期刊>Journal of neurological sciences (Turkish) >Audiogenic Seizures Potentiate Hippocampal Neuronal Loss in Ethanol-Dependent Rats
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Audiogenic Seizures Potentiate Hippocampal Neuronal Loss in Ethanol-Dependent Rats

机译:音源性癫痫发作可增强乙醇依赖大鼠的海马神经元损失

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Objective :Audiogenic seizure (AS) susceptibility is observed following withdrawal from chronic ethanol treatment in rodents. This is the first study to investigate and compare the effects of ethanol withdrawal on the hippocampal formation in AS appeared and non-appeared animals. Material and Methods :Adult male Wistar rats (225-320 g) were used. Ethanol was given to rats in a modified liquid diet for twenty days. Daily ethanol consumption was in a range of 10.35±1.25 to 15.20±0.79 g/kg during the exposure to ethanol (7.2%). At the end of exposure to a 7.2% ethanol-containing liquid diet, ethanol was withdrawn and withdrawal signs were recorded or rated. Increased stereotyped behavior, wet dog shakes, agitation, tail-stiffness and abnormal posture and gait appeared during ethanol withdrawal in dependent rats. AS was also induced in 5 of 11 of ethanol dependent rats. Following audiogenic stimuli, rats were decapitated and their brains were removed. Neuron counts from pyramidal cell layers in CA1 and CA2-3 regions of the hippocampus were obtained from control rats and ethanol-dependent rats with and without audiogenic seizure. Results :Significant neuronal losses were found in CA1 and CA2-3 regions of the hippocampal formation in the ethanol-dependent group. Neuronal loses in AS appeared group were significantly more than in AS non-appeared group. Conclusions :ASs during ethanol withdrawal significantly potentiated neuronal degeneration in all subdivisions of the CA area of the hippocampal formation in rats. Thus, prevention of seizures in alcoholic individuals may be important for protection from excessive neuronal damage in the hippocampus.
机译:目的:在啮齿类动物中退出长期乙醇治疗后观察到音源性癫痫发作(AS)敏感性。这是第一个研究和比较乙醇戒断对AS出现和未出现动物的海马形成影响的第一项研究。材料与方法:使用成年雄性Wistar大鼠(225-320 g)。用改良的流质饮食给大鼠乙醇二十天。暴露于乙醇(7.2%)期间,每日乙醇消耗量为10.35±1.25至15.20±0.79 g / kg。暴露于7.2%的含乙醇流质饮食结束后,撤出乙醇,并记录或评估撤出迹象。在依赖酒精的大鼠戒断乙醇期间,其刻板印象行为增加,狗湿摇,躁动,尾巴僵硬,姿势和步态异常。 11只乙醇依赖大鼠中有5只还诱导了AS。听觉刺激后,将大鼠断头并切除大脑。海马CA1和CA2-3区锥体细胞层的神经元计数是从有或没有发源性癫痫发作的对照大鼠和乙醇依赖性大鼠中获得的。结果:乙醇依赖性组海马CA1和CA2-3区域神经元明显丢失。 AS出现组神经元丢失明显多于AS未出现组。结论:乙醇撤除期间的ASs在大鼠海马形成CA区所有子区均显着增强了神经元变性。因此,预防酒精中毒者的癫痫发作对于保护海马免受过度的神经元损害可能是重要的。

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