谷氨酸及其受体在局灶性皮质发育不良模型大鼠大脑皮质中的表达

Expression of glutamate and its receptors in cerebral cortex of rats with focal cortical dysplasia

目的观察液氮损伤诱发局灶性皮质发育不良模型大鼠大脑皮质中谷氨酸(Glu)及N-甲基-D-天冬氨酸受体1(NMDAR1)、谷氨酸受体2(GluR2)的表达,探讨其表达情况与癫痫发作的关系及可能的发病机制。方法纳入36只大鼠,随机分成正常对照组、假手术组及手术组,创建局灶性皮质发育不良大鼠模型,HE染色,免疫组织化学方法(用SABC法)检测微脑回神经递质及受体变化,使用SAS 8.0统计学软件进行数据分析。结果手术组经液氮铜针处理,在大鼠损伤处形成微脑回畸形,畸形处皮质层Glu及NMDAR1、GluR2免疫阳性着色神经元表达较正常组及假手术组有所增多,光密度值比较差异无统计学意义(P>0.05),然而在微脑回皮质周围见到Glu及NMDAR1、GluR2免疫阳性着色神经元表达较正常组及假手术组有显著增加,光密度值比较差异亦有统计学意义(P<0.05),其他海马及杏仁核等脑区没有明显改变。结论微脑回畸形周围兴奋性神经递质Glu及其受体的增加可能是导致癫痫发生的机制之一。

Objective To observe the expression of glutamate and its receptors(NMDAR1 and GluR2)in the cerebral cortex of rats with focal cortical dysplasia induced by liquid nitrogen and explore the association of their expression levels with epilepsy and its possible pathogenesis.Methods Thirty six rats were randomly divided into normal control,sham and operation groups.The rat model of focal cortical dysplasia was established.The changes of neurotransmitters and receptors in the microgyrus were detected by HE staining and Strept Avidin-Biotin Complex(SABC)immunohistochemical staining.SAS 8.0 statistical software was used for statistical analysis.Results After treating with copper needles chilled by liquid nitrogen,microgyrus deformity was formed in the injured part in operation group.In the cortex of the microgyrus deformity sites,the expression of Glu,NMDAR1 and GluR2 immunopositive neurons were more in operation group than that in normal control or sham groups,but there was no significant difference in optical density among three groups(P>0.05).However,in the surrounding of the cortex of the microgyrus deformity sites in operation group,staining neurons were increased relative to normal control or sham groups,and there was a significant difference in optical density among three groups(P<0.05).The expression levels of Glu,NMDAR1 and GluR2 were not significantly changed in other brain regions such as hippocampus and amygdala.Conclusion The increase of excitatory neurotransmitter glutamate and its receptors around microgyrus malformation may be one of the mechanisms leading to epilepsy.