摘要
目的：探讨大脑皮质发育不良（DCD）大鼠大脑半球、海马的免疫组化病理学特点及其所致难治性癫痫（IE）的发生机制。方法：建立X-射线照射诱导的皮质下异位结节大鼠DCD模型，采用SP免疫组织化学方法检测神经元特异核蛋白抗原（NeuN）和星形胶质细胞特异抗原（GFAP）在大鼠脑皮质下和海马中异位结节的表达，阳性细胞计数，用SPSS10．0软件统计。结果：DCD组与正常对照或母鼠组白质比较，皮质下异位结节内NeuN免疫阳性神经元和GFAP免疫阳性细胞数密度分别增加30倍和16倍，差异有统计学意义（P〈0．05）。同龄而不同部位DCD病变组间脑皮质Ⅰ～Ⅲ层异位结节、皮质下异位结节和CA1区异位结节中NeuN、GFAP免疫阳性细胞数密度或阳性平均光密度值比较，差异无统计学意义。结论：DCD鼠脑NeuN及GFAP的分布证实了皮质下异位结节的内在属性，异位结节是灰质，主要是由神经元和星形胶质细胞构成。
Objective：To observe the routine pathological characteristics of animal models of diffuse cortical dysplasias（DCD） in cortex by the immunohistochemical method, and to observe the behavioral character, EEGs and seizure susceptibility, and discuss the mechamism of pathologic changes and epileprogenesis in the modelsl Methods：By immunohistochemicai method DCD models of rats were examined in NeuN and GFAP including those of Postnatal P0, P1, P2, P3, P7, P14, P21, P28, P56, P84 and 31 weeks. The offsprings of irrated pregnant rats were killed for histomorphology and histopathologic studies. The expressions of NeuN,GFAP in cortex and hippocampus were observed by immunohisochemistry. Statistic analysis by mean standard deviation（x±s）, P〈0.05 represented significance, student test analysis or nonparametric Kruskal-Wallis H test and Nemenyi test in SPSS 10.0 were einployed. Results： The expressions of NeuN and GFAP in cortex and hippocampi CA1 ,CA3 area were reprasented by immunohisochemistry. The CA1 density of NeuN and GFAP 30 times and 16 times increased respectively. Neun and GFAP around DCD in white matter of DCD rats might have relationship with the mechanisms of the intractable epilepsy （P〈0.05）. Conclusion： Application of the immunohistochemical methods to study expression of NeuN and GFAP exhibits internal attribution of ectopia nodus, as grey matter, mainly be made up of neurons and horizontal cells.
出处
《癫痫与神经电生理学杂志》
2012年第4期193-196,201,F0003,共6页
Journal of Epileptology and Electroneurophysiology(China)
基金
四川省教育厅重点项目（编号：09ZA046）
四川省卫生厅项目（编号：090231）
泸州市科技局项目[泸市科计（2009）1号]
泸州医学院青年基金项目（编号：09013）
泸州医学院附属医院人才基金项目（编号：09057）资助
