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目的探讨Fmr1基因敲除小鼠的学习记忆功能和海马的谷氨酸脱羧酶(GAD)表达变化的关系。方法对4周龄和6周龄的基因敲除型(KO)鼠和野生型(WT)鼠分别连续进行2天的被动回避行为的避暗和跳台实验观察后使用免疫印迹技术检测海马GAD的表达变化,根据所获得的数据进行多因素方差分析处理。结果避暗实验中,4周龄和6周龄KO鼠潜伏期比WT鼠明显少(P<0.05);而KO鼠的错误次数比WT鼠明显多(P<0.05);4周龄和6周龄KO鼠或WT鼠的潜伏期、错误次数无差异(P>0.05),同周龄WT鼠第一天的潜伏期和错误与第二天相比无差异(P<0.05)。跳台实验中,4周龄和6周龄KO鼠的潜伏期比WT鼠明显少(P<0.05);而KO鼠的错误次数比WT鼠明显多(P<0.05);4周龄和6周龄KO鼠或WT鼠的潜伏期、错误次数无差异(P>0.05);同周龄第一天KO鼠的潜伏期和错误次数与第二天相比无差异(P>0.05);同周龄第一天WT鼠的潜伏期和错误次数与第二天相比有显著差异(P<0.05)。GAD65/67蛋白在KO鼠海马表达比WT鼠增多(P<0.05);随着周龄的增加,6周龄KO鼠或WT鼠的GAD65/67蛋白表达比4周龄表达增多(P<0.05)。结论 4周龄和6周龄Fmr1基因敲除小鼠存在认知功能障碍,海马的GAD的表达异常变化可能介导Fmr1基因敲除小鼠学习记忆障碍。
Objective To investigate the relationship between learning and memory function and glutamate decarboxylase (GAD) expression in Fmr1 knockout mice. Methods Two-day passive avoidance behaviors of 4-week-old and 6-week-old knockout (KO) mice and wild-type (WT) mice were observed and observed by step-down test. Western blotting was used to detect GAD Expression changes, according to the data obtained by multiple factor analysis of variance. Results In the dark-avoidance experiment, the latency of KO rats at 4 weeks and 6 weeks was significantly less than that of WT mice (P <0.05), while that of KO mice was significantly higher than that of WT mice (P <0.05) There was no significant difference in the number of latencies and errors in KO mice or WT mice (P> 0.05). There was no difference in latency and error between the first day and the second day of WT mice (P <0.05). In the step-down test, the latency of KO rats at 4 weeks and 6 weeks was significantly lower than that of WT mice (P <0.05), while that of KO rats was significantly higher than that of WT mice (P <0.05) There were no significant differences in latency and number of errors between KO mice and WT mice (P> 0.05). There was no significant difference in the latency and number of errors of KO rats on the first day of the same week compared with the second day (P> 0.05) There was a significant difference (P <0.05) in the latency and error of WT rats compared with the second day. The expression of GAD65 / 67 protein in hippocampus of KO rats was higher than that of WT rats (P <0.05). The expression of GAD65 / 67 protein in 6-week-old KO mice or WT mice was higher than that of WT rats ). Conclusion Fmr1 knockout mice at 4 weeks and 6 weeks have cognitive dysfunction. The abnormal expression of GAD in hippocampus may be mediated by learning and memory impairment in Fmr1 knockout mice.