摘要
目的:探索与鼠同源的人类已知基因在苯妥英钠耐药和非耐药癫痫鼠脑中的差异表达,了解难治性癫痫形成(PHT)机制。方法:建立耐药和非耐药组癫痫大鼠模型,成功后,处死动物,取出脑组织,常规抽提,逆转录生成PHTmRNAcDNA后,应用含有条人类基因的表达谱芯片,检测两者间基因表达谱的差异。4096cDNA结果:发现耐和治疗有效癫痫PHTPHT鼠与神经元突触可塑性有关的基因有条存在差异表达。18结论:突触可塑性增强可能是难治性癫痫形成的重要原因。
Objective: To determine the differential synapse plasticity-associated gene expression in PHT-resistant and PHT-responder epilepsy rat brain. Methods: Phenytoin-resistant and phenytoin-responder epilepsy rat model was build and the genes expression associated with synapse plasticity by cDNA microarray were studied. The four thousand and ninety-six target genes were arrayed onto glass slide. Both the mRNA from phenytoin-resistant and phenytoin-responder brains of kindling rats were reversal transcribed to cDNAs as hybridization probes which were labeled with either Cy3-dUTP or Cy5-dUTP at the same time. After hybridization with BioDoor4096 cDNA microarray, the results were analyzed by ImaGene3.0 software. Results: In the PHT- resistant and non-resistant epileptic rats, eighteen differential expressed genes which are associated with snapse plasticity were identified. Conclusion: The enhancement of synapse plasticity may be one of the important causes of drug-resistant epilepsy.
出处
《重庆医科大学学报》
CAS
CSCD
2002年第3期276-279,共4页
Journal of Chongqing Medical University
关键词
基因芯片
难治性癫痫
突触可塑性
cDNA microarray
Intractable epilepsy
Synapse plasticity