Background It is known that excessive release of glutamate can induce excitotoxicity in neurons and lead to seizure. Dexamethasone has anti-seizure function. The aim of this study was to investigate glutamatedexamethasone interaction in the pathogenesis of epilepsy, identify differentially expressed genes in the hippocampus of glutamate-induced epileptic rats by mRNA differential display, and observe the effects of dexamethasone on these genes expression. Methods Seizure models were established by injecting 5μl （250 μg/μl） monosodium glutamate （MSG） into the lateral cerebral ventricle in rats. Dexamethasone （5 mg/kg） was injected intraperitoneally at 30 minutes after MSG inducing convulsion. The rats＇ behavior and electroencephalogram （EEG） were then recorded for 1 hour. The effects of dexamethasone on gene expression were observed in MSG-induced epileptic rats at 1 hour and 6 hours after the onset of seizure by mRNA differential display. The differentially expressed genes were confirmed by Dot blot. Results EEG and behaviors showed that MSG did induce seizure, and dexamethasone could clearly alleviate the symptom, mRNA differential display showed that MSG increased the expression of some genes in epileptic rats and dexamethasone could downregulate their expression. From more than 10 differentially expressed eDNA fragments, we identified a 226 bp eDNA fragment that was expressed higher in the hippocampus of epileptic rats than that in the control group. Its expression was reduced after the administration of dexamethasone. Sequence analysis and protein alignment showed that the predicted amino acid sequence of this cDNA fragment kept 43% identity to agmatinase, a member of the ureohydrolase superfamily. Conclusions The results of the current study suggest that the product of the 226 bp eDNA has a function similar to agmatinase. Dexamethasone might relax alleviate seizure by inhibiting expression of the gene.
MA Chun-lingZHU Chang-gengFAN MingLIU Shu-hongLIU Qing-yingCONG Bin
Intracellular recording method of electrophysiology was used to study the effect of microinjection of coriaria lactone (CL) into hippocampus on membrane potential of hippocampal neurons in rats. The membrane potential in 34 neurons of 12 rats were recorded. The results showed that CL induced depolarization of all of 34 neurons examined. Among the 34 neurons, 15 had paroxysmal depolarization accompanied by spike discharge in cluster and spike discharge in cluster ceased when membrane was hyperpolarized, 7 showed continuous depolarization accompanied by continuous spike discharge and 12 had only depolarizing response. The results suggest that injection of CL into hippocampus may lead to an increase of excitability of local neurons accompanied by different patterns of epileptioform discharge.
目的:为获得癫痫患者免疫学异常的证据,本实验检测了患者血清中抗脑抗体(Anti-encephalic antibodies,AEAb)及脑组织人类白细胞抗原Ⅱ类抗原(Human leukocyte antigen class Ⅱantigen,HLA class Ⅱ antigen,HLA-Ⅱ类抗原),并与正常对照组比较。对象及方法:1.用ELISA方法测定37例癫痫患者血清抗脑自身抗体;2.借助免疫组织化学方法观察了HLA—Ⅱ类抗原在脑组织中表达与分布。结果:1.癫痫患者血清抗脑抗体高于正常对照;2.癫痫患者脑组织中星形胶质细胞和小胶质细胞异常表达HLA—Ⅱ类抗原。讨论:本实验证实癫痫患者存在一定程度的自身免疫应答异常。脑组织胶质细胞表面HLA—Ⅱ类抗原表达异常可能通过多种机制参与癫痫发病。
