摘要癫痫是一种由于大脑神经元突发性异常放电，导致短暂的大脑功能障碍的一种慢性疾病，在国内成为仅次于头疼的第二大常见疾病。近几年关于癫痫研究的进展取得长足进步。癫痫领域研究进展包括以下几点：癫痫基因及致病机制，抗癫痫药物对神经发育的影响，依赖闭环神经刺激系统治疗癫痫方法。这些成果对临床实践和未来研究都有重要意义。以近些年有关癫痫小鼠模型的研究成果为依据，开展本次实验。74248

目的 基于PV神经元异常的癫痫小鼠模型的构建。 方法 使用genotyping鉴定出Parvalbumin-tTA与TetRE-caErbB2杂交后代中癫痫小鼠的基因型，通过WB鉴定小鼠大脑各脑区神经元和胶质细胞特异蛋白表达量，并使用IF鉴定各种胶质细胞和神经元的分布和数量。 结果 出生57天停药36天的PV+ErbB2+小鼠，1个月大时表型弱小，四肢无力，偶发癫痫症状，解剖后发现内脏明显小于对照组PV- ErbB2+小鼠。WB显示小鼠大脑各脑区神经元和胶质细胞特异蛋白表达量没有明显变化，IF显示PV- ErbB2+与PV+ ErbB2+的各部位各种胶质细胞和神经元的分布和数量没有显著变化。 结论 这种使用Tet-off系统构建的能够特异的活化ErbB2信号通路的PV阳性神经元小鼠，经过WB与IF证明PV细胞的数量和分布没有明显差异，猜测可能是PV细胞功能发生改变，从而使得小鼠产生癫痫症状。

Abstract Epilepsy as a result of sudden abnormal discharge of neurons in the brain, leading to brain dysfunction of the short is a chronic disease, became second only to headache in the country's second-largest common diseases。 On progress in Epilepsy Research has made great progress in recent years。 Advances in the field of epilepsy include the following: gene and pathogenesis of epilepsy, antiepileptic drug effects on neurodevelopment, relying on closed loop neural stimulation system in the treatment of epilepsy。 These results have important significance for clinical practice and future research。 In recent years relating to epilepsy in mice models based on the research results, carried out this experiment。

Objective  based on PV abnormal neurons of mouse model of epilepsy。 Method  uses genotyping to identify Parvalbumin-tTA and TetRE-caErbB2 hybrid genotypes of epilepsy in mice, by WB identification of mouse brain regions of the brain neurons and glial cell-specific protein expression and use IF to identify the distribution and abundance of glial cells and neurons。 Results  born 57 days and discontinuation 36 days  PV+ErbB2+ mice, when 1-month-old it was weak, limp, occasional epileptic symptoms, autopsy found internal organs was significantly less than the control group after PV-ErbB2+ in mice。 WB show mouse brain regions of the brain neurons and glial cell-specific protein expression did not change significantly, IF shows various parts of PV-ErbB2+ and PV+ ErbB2+ a variety of glial cells and the distribution and no significant change in the number of neurons。 Conclusion  this Tet-off system is built to specifically activate ErbB2 signaling pathways of PV-positive neurons in mice, proved by WB and IF the number and distribution of PV cells there was no significant difference, suspect it could be a function change of PV cells, making symptoms of epilepsy in mice。

毕业论文关键词：癫痫; PV+神经元; ErbB2信号通路; Tet-off

  Key words:  Epilepsy;  PV+ neurons;  ErbB signaling pathway;  Tet-off 

目录

摘要。2

目录。3

1、前言4

1。1癫痫小鼠模型的研究进展4

1。2预设实验流程图5

2、基于PV神经元异常的癫痫小鼠模型的构建。 5

2。1实验材料5

2。1。1实验动物5

2。1。2药品5

2。1。3实验仪器6

2。1。4实验耗材6