中文摘要：

目的：探讨脂蛋白酯酶（LPL）基因mRNA在精神分裂症模型大鼠前脑皮层、杏仁核、尾壳核和海马4个脑区中的表达,阐明其在精神分裂症发病中的作用机制。方法：选择围产期Wistar大鼠,模型组24只,对照组21只,建立苯环已哌啶（PCP）处理的大鼠精神分裂症动物模型,通过Morris水迷宫实验验证动物模型是否建立成功,并检测其认知改变,采用实时荧光定量PCR法检测LPL基因mRNA在精神分裂症模型大鼠前脑皮层、杏仁核、尾壳核和海马4个脑区中的表达。结果：Morris水迷宫实验,与对照组比较,模型组大鼠找到平台的时间明显延长,为对照组的4.25倍（P〈0.01）;与对照组比较,模型组大鼠脑组织中前脑皮层和海马区LPL mRNA表达水平降低,分别下降了61.7%和89.0%（P〈0.05）。结论：LPL基因在大鼠前脑皮层和海马表达水平降低可能与精神分裂症有关联,并且可能与认知障碍存在一定的联系。

英文摘要：

Objective： To explore the expressions of lipoprotein lipase （LPL） gene mRNA in the prefrontal cortex, amygdale, caudate-putamen and hippocampus tissues of the model rats with schizophrenia, and to clarify the mechanism in the pathogeneses of schizophrenia. Methods.. The rat modes with schizophrenia were made by administing phencyclidine （PCP） to the prenatal rats. 24 model rats were used as model group, and another 21 Wistar rats were used as control group. The models were certified and the cognition changes were detected by Morris water maze test. The expression levels of LPL gene mRNA in the prefrontal cortex, amygdale, caudateputamen and hippocampus tissues of the model rats with schizophrenia were tested by Real-Time PCR. Results.. In Morris water maze test, the time of arriving at the platform of the rats in model group was 4.25 times longer compared with control group （P〈0.01）. The mRNA expression levels of LPL gene decreased in prefrontal cortex and hippocampus of the rats in model group were decreased by 61.7% and 89.0% compared with control group （P〈0.05）. Conclusion： The decreasing of LPL gene expression levels in the prefrontal cortex and hippocampus tissues of the model rats may be associated with the pathogenesis of schizophrenia, and it may he related to the cognition disorder.