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中文摘要：
目的：采用高通量基因芯片观察大鼠抑郁症模型基因表达的变化,结合基因功能分类体系探讨抑郁症的发病机制.方法：实验于2004-04/2005-10在成都康弘集团实验动物中心和哈尔滨医科大学完成.采用Willner法对32只雄性SD大鼠构造大鼠抑郁症模型,应激刺激造模结束后将大鼠分为模型组和正常组,每组各8只.由基因芯片检测8只模型组和8只正常组大鼠的基因表达谱,识别差异表达基因并注释于GO基因功能分类体系,分析差异表达基因与疾病的相关性.结果：实验纳入大鼠数量为16只,实验中无意外死亡、丢失及补充,进入结果分析大鼠数量为16只.对模型组和正常组,通过t检验筛选得到207个差异表达基因,涉及神经肽激素活性、信号传导通路、核糖体生成以及蛋白质转运与降解.具有钙调蛋白依赖的蛋白激酶活性基因钙调蛋白依赖的蛋白激酶1、钙调蛋白依赖的蛋白激酶2G、钙调蛋白依赖的蛋白激酶2抑制物α、具有囊泡介导转运功能的基因突触蛋白表达下调也表明这些通路在大鼠抑郁症模型中可能被抑制;有神经肽激素活性的精氨酸加压素表达下凋,验证了情感性精神障碍的精氨酸加压素的假说,即抑郁症患者精氨酸加压素功能降低,在躁狂症患者则升高.进一步验证了抑郁症的病理机制所涉及的可能是神经传递功能的多个环节.结论：单胺递质的释放、信号传导以及神经肽调节的表达变化涉及抑郁症的发病机制,提示多种功能通路与抑郁症的发病机制相关.
英文摘要：
AIM： To observe the alteration of gene expression of depression rat models by gene chips of high flux, and explore the pathogenesis of depression combining with classification system of gene function. METHODS： The experiment was conducted at the Experimental Animal Center of Chengdu Kanghong Group and Harbin Medical University between April 2004 and October 2005. Thirty-two male SD rats were selected for establishing depression models by Willner method, and divided into model group and normal group after stress stimulation, with 8 rats in each group. Gene expression profiles were measured in both groups by gene chips. Differentially expressed genes were identified and annotated to Gene Ontology （GO） database in order to analyze the correlation of disease and differentially expressed genes. RESULTS： There were 16 rats in the experiment without accidental death, loss or supplement, and finally entered the result analysis. A total of 207 differentially expressed genes were screened through t test, and generally related to neuropeptide hormone activity, signaling pathway, ribosome biogenesis as well as protein transport and degeneration. Calmodulin-dependent protein kinase Ⅰ activity associated genes calmodulin-dependent protein kinase Ⅰ （Camkl）, calmodulin-dependent protein kinase Ⅱ G （Camk2G）, calmodulin-dependent protein kinase Ⅱ inhibitor alpha and veside-mediated transport activity associated gene synapsin （Synl） down-regulated, which suggested that the pathways were possibly suppressed in depression models. Decreased expression of neuropeptide hormone activity associated gene arginine vasopressin （AVP） validated the AVP hypothesis for affective disorder, in other words, the function of AVP was reduced in depression patients while enhanced in mania ones. These results further verified that the pathogenesis of depression might be associated with several steps of neurotransmission. CONCLUSION： The gene expression alteration of release and signal transduction of monoamine and the
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