中文摘要：

目的 探讨微白蛋白（PV）阳性中间神经元在脆性X综合征（FXS）癫痫易感性增加中的作用. 方法 应用免疫组织化学染色检测FVB近交系雄性2、4、6 W龄FMR1基因敲除型（KO）（KO2W、KO4W、KO6W）和同龄野生型（WT）（WT2W、WT4W、WT6W）小鼠大脑纹状皮质、颞听皮质、梨状皮质及海马CA1区、CA3区、齿状回中PV的表达（n=6）;应用Western blot法检测上述小鼠大脑皮层、海马组织PV的含量（n=6）. 结果 KO2W、KO44W小鼠的大脑纹状皮质、颞听皮质、梨状皮质、海马CA1和CA3区PV阳性中间神经元的数量分别较WT2W、WT4-小鼠减少,差异有统计学意义（P〈0.05）;KO2W和KO4W小鼠大脑皮层、海马中PV含量分别较WT2W、WT4W小鼠减少,差异有统计学意义（P〈0.05）. 结论 PV阳性中间神经元及PV含量的减少.可能是引起FXS模型鼠癫痫易感性增加的主要原因.

英文摘要：

Objective To explore the possible role of parvalbumin （PV）-positive interneuron in the pathogenesis of increased susceptibility to epileptic seizures in FMR1 gene knockout （FMR1 KO）mice. Methods Immunohistochemistry was employed to determine the expression of PV in CA1 and CA3 regions of the hippocampus, the striate cortex, the temporal auditory cortex and the piriform cortex of FVB strain FMR1 KO mice and wild type （WT） controls at the age of 2, 4 and 6 w. Western blotting was used to detect the level of PV in the cerebral cortex and hippocampus of the above mice. Results The numbers of PV-positive interneuron in CA1 and CA3 regions of the hippocampus, the striate cortex,the temporal auditory cortex and the piriform cortex of FMR1 KO mice at the age of 2 and 4 w were significantly decreased as compared with those in the age-matched WT mice （P〈0.05）. The level of PV in the cerebral cortex and hippocampus in FMR1 KO mice at the age of 2 and 4 w was also significantly decreased than that in the age-matched WT mice （P〈0.05）. Conclusion Decreased numbers of PV-positive interneuron and level of PV might induce the increased susceptibility to epileptic seizures inFMR1 KO mice.