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The Effect of Binge Drinking Treatment on Nom-synaptic Epileptiform Activities

机译:狂犬病饮用处理对Nom-Synaptic癫痫型活性的影响

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Non-synaptic mechanisms have been related to the onset of epileptic seizures and brain damage caused by alcohol intoxication. To understand this relationship, adult male Wistar rats, between 300 and 350 g, were submitted to the binge drinking alcohol protocol, receiving ethanol every 8 h for 4 consecutive days intragastrically. Part of the animals developed status epilepticus about 12 h after the last dose of ethanol. Changes in the immunoreactivity of the cation-chloride co-transporters (NKCC1 and KCC2), NaV K+-ATPase enzyme and astrocytic reactivity (GFAP expression) of alcoholic animals with and without seizures and control animals were investigated. Immunohistochem-ical analyzes were compared to electrophysiological recordings of non-synaptic epileptiform activity induced in hippocampal slices. The results show that the periodic and abusive use of alcohol is associated with imbalances of the ionic homeostasis in the brain, leading to serious osmotic variations related to neuronal and glial swelling, with concomitant cellular loss, which hinders synchronization processes, especially after status epilepticus.
机译:非突触机制已与癫痫发作和由酒精中毒引起的脑损伤的发作有关。要了解这种关系,成年男性Wistar大鼠300至350克,提交到狂犬病饮酒方案,每8小时胃肠每8小时接受乙醇。一部分动物在最后剂量的乙醇后开发了9小时的状态癫痫症。研究了含有癫痫发作和对照动物的持阳氯共转运蛋白(NKCC1和KCC2),NAM K + -ATP酶和星形胶质反应性(GFAP表达)的阳离子 - 氯化物共转运蛋白(NKCC1和KCC2),NAV K + -ATP酶和星形胶质反应性(GFAP表达)。将免疫组织分析与海马切片中诱导的非突触癫痫活性的电生理记录进行比较。结果表明,醇的周期性和滥用使用与大脑中离子稳态的失衡有关,导致与神经元和胶质肿胀有关的严重渗透变化,伴随着细胞损失,妨碍了同步过程,特别是在状态癫痫后。

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