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 5 μl (250μg/μl) monosodium glutamate (MSG) into the lateral cerebral ventricle in rats. Dexamethasone (5mg/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 cDNA fragments, we identified a 226 bp cDNA 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 cDNA has a function similar to agmatinase. Dexamethasone might relax alleviate seizure by inhibiting expression of the gene.

目的研究三七总皂甙（panaxnoto ginsengsa ponins，PNS）对吗啡戒断大鼠海马神经细胞内[Ca2+]i的影响，探讨PNS缓解吗啡戒断症状的可能机制。方法应用剂量递增法大鼠皮下注射吗啡及腹腔注射纳络酮建立吗啡躯体依赖及催促戒断模型。在给予吗啡的同时分别以PNS100、200、400mg/kg对大鼠灌胃，记数大鼠的体质量变化和跳跃次数以确定模型建立是否成功，采用流式细胞术测定其海马神经细胞内[ca2+]i浓度。结果①PNS呈剂量依赖性抑制戒断大鼠体质量减轻和跳跃的发生，②慢性吗啡作用可以使海马神经细胞内[Ca2+]i明显升高；纳络酮可迅速下词这种异常增高的[Ca2+]i；PNs则可增加纳络酮催促戒断大鼠海马神经细胞内[Ca2+]i，且呈剂量依赖性。结论PNS可能通过调节神经细胞内[Ca2+]i，抑制吗啡依赖大鼠催促戒断症状的发生。

目的建立一套安全、经济、可靠的实验条件。为检测大鼠海马μ阿片受体奠定方法学基础。方法从膜蛋白提取、结合反应体系、孵育温度、孵育时间等方面，对放射配基结合分析的实验条件进行摸索；并从环保、经济的角度考虑。对实验进行了优化。结果发现当蛋白浓度为1mg/mL、[3H]DAMGO0.5～8.Onmol/L5个浓度点、非标记配基DAMGO浓度为5μmol/L、4℃孵育过夜的条件下，结果稳定、可靠。结论该方法经济、可靠、重复性好。且易于掌握、污染少。

目的：研究三七总皂甙（PNS）对吗啡戒断大鼠大脑皮质m2，m5乙酰胆碱受体（AChR）mRNA及蛋白表达的影响，探讨PNS抑制吗啡戒断症状的作用机制。方法：以剂量递增法建立大鼠吗啡依赖模型（MOR组），以腹腔注射（ip）纳洛酮建立催促戒断模型（NAL组），大鼠在给予吗啡的同时，采用3种不同剂量PNs（100、200、400mg?kg-1）灌胃（ig）。采用RT-PCR和Westem-blot方法分别观察PNs对吗啡依赖及戒断大鼠皮质m2，m5AChRmRNA及蛋白表达的影响。结果：（1）慢性吗啡作用使皮质m2，m5AchRmRNA及m2AchR蛋白表达明显增加（P<0.01）；（2）纳洛酮催促戒断使m2，m5AChRmRNA及蛋白表达进一步升高（P<0.01）；（3）PNS可以剂量依赖性地抑制纳洛酮催促戒断所引起的AchRmRNA及蛋白表达的增强。结论：PNS可通过抑制m2，m5AChRmRNA及蛋白的表达缓解吗啡戒断症状。