摘要
目的:探讨缺氧性脑损伤后亚临床癫痫发作及其与胶质原纤维酸性蛋白的关系。方法:成年雄性SD大鼠,随机分为对照组与缺氧组,以8%氧氮混合气体缺氧,通过监测大鼠脑电活动,又将缺氧大鼠分成亚临床发作组与非亚临床发作组、分别用Nissle染色、免疫组织化学和免疫蛋白印迹等技术观察皮层、海马的神经病理学改变以及检测海马组织胶质原纤维酸性蛋白(Glial fibrillary acidic protein,GFAP)表达。结果:大鼠缺氧损伤后部分大鼠出现尖波、尖慢波和棘波,痫样放电的发生率为19.67%。较非亚临床发作组,亚临床发作组海马CA1、CA3区、颞叶皮质神经元脱失明显(P<0.05)。亚临床发作组GFAP表达明显增强,以海马为著,与非亚临床发作组比较差异有显著性(P<0.05)。结论:成年大鼠缺氧性脑损害后可出现痫样放电,并与脑内GFAP表达增加和神经元脱失有关。
Objective:To explore the mechanism of early onset subclinical seizures following hypoxic brain injury. Methods:SD male adult rats were assigned randomly to control rats and rats exposed to global hypoxia by 8% oxygen nitrogen atmosphere. According to electroencephalogram recording seizure discharge,hypoxic rats were divided into subclinical seizures group and non-subclinical seizures group,then the changes in neuropathology and the expression of GFAP in cortex and hippocampus of rat brain were studied by Nissle-staining ,immunohisochemistry and western-blot. Results:Subclinical seizures occurred in 19.67% rats following hypoxia. Compared with non-subclinical seizure group,neuronal loss of hippocampal CA1 and CA3 region as wel as temporal cortex were distinct in subclinical seizure group(P〈0.05). Meanwhile,the expresssion of GFAP in subclinical seizure group was stronger than that of non-subclinical seizure group,especially in hippocampal area(P〈0.05). Conclusion:Onset subclinical seizures occured following hypoxic injury in adult rats,which may be related to increased GFAP expression and neuronal loss following hypoxic brain damage .
出处
《重庆医科大学学报》
CAS
CSCD
2007年第12期1256-1259,1319,共5页
Journal of Chongqing Medical University