中文摘要：

目的探讨脆性X综合征中钙结合蛋白Calbindin在神经元树突棘形态异常中的作用。方法我们选用FVB品系的FMR1基因敲除型（KO）和野生型（WT）小鼠，分别取新生l、3、5、7、10、14d，及成年（6周）的KO小鼠以及WT小鼠用免疫组织化学方法检测钙结合蛋白Calbindin在脑组织中的分布和表达情况，分别对大脑纹状皮质、海马、颞叶听区、梨状皮质、丘脑及小脑的免疫阳性显色细胞进行检测。结果在新生1d龄WT型及KO型小鼠中Calbindin免疫阳性细胞首先出现于梨状皮质和小脑皮质中，随着天龄的增长脑内其他各区逐渐出现Calbindin免疫阳性细胞的表达．且≤10d KO型小鼠Calbindin免疫阳性细胞平均光密度均显著高于WT型小鼠（P〈0．05）。结论FMRP通过负性调节脑内钙结合蛋白Calbindin的表达，这推测与FMR1基因敲除小鼠神经元树突和树突棘形态异常有关。

英文摘要：

Objective Through studying distribution and expression of calcium combined with protein-Calbindin in postnatal rat brain tissue knocked off by FMR-1 gene and comparing with wild rats of the same strain, we discuss the role of Calbindin in dendrite spines of neuron of fragile X syndrome. Methods The distribution and expression of Calbindin in brain tissue were detected in the way of immunohistochemistry with KO little rats with the age of 1, 3, 5, 7, 10, 14 days and adult rat with the age of 6 weeks and WT little rat in the ranges of FMR-1 gene knockout （KO） rat＇s and wilt （WT） rat＇s brain from FVB series. The positive immunohistochemistry cells were tested in the regions of brain striated cortex, temporal lobe, pyriform cortex, hippocampus and cerebellar cortex respectively. Results The positive immunohistochemistry cells of WT rat and little rat of 1 day first expressed in pyriform cortex and cerebellum cortex in plday and then expressed in other important brain regions like neocortex, hippocampus, thalamus as rats grow up. And the average optical density in KO rats with the age of no more than 10 days is more than that in WT rats （P〈0.05）. Conclusion The speculation that FMRP modulates distribution and expression of the calcium combined with protein-Calbindin negatively could have some relationship with abnormal morphology of dendrite spines and dendrite of neuron in FMR-1 gene knockout rat.