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目的对不同年龄Fmr1基因敲除小鼠的听源性惊厥行为观察。方法使用PCR技术对Fmr1基因敲除小鼠鉴定后对不同周龄的Fmr1基因敲除小鼠和野生型小鼠进行听源性惊厥的观察,数据采用多因素方差分析处理。结果经PCR技术证实脆性X综合征小鼠模型是Fmr1基因敲除小鼠。Fmr1基因敲除小鼠在中央区的惊厥阈值较野生型小鼠显著短。Fmr1基因敲除小鼠鼠受声音刺激后表现为惊恐、奔跑明显的AGS前驱表现,最后发生跌倒、惊厥,呈角弓反张状,最后恢复活动能力或者反复发作,或者导致死亡。结论 Fmr1基因敲除小鼠的行为异常,其兴奋性较野生型小鼠增高。
Objective To investigate the auditory convulsion behavior of Fmr1 knockout mice of different ages. Methods Fmr1 gene knockout mice were identified by PCR and their auditory convulsions were observed in Fmr1 knockout mice and wild type mice at different weeks of age. The data were analyzed by multivariate analysis of variance. Results Confirmed that the mouse model of Fragile X syndrome was Fmr1 knockout mice by PCR. Fmr1 knockout mice in the central area of the seizure threshold was significantly shorter than wild-type mice. Fmr1 knockout mice were stimulated by sound to appear panic-stricken, running significantly AGS precursor manifestations, finally falling, convulsions, angular arch anti-Zhang Xing, the final recovery activity or recurrent, or lead to death. Conclusion Fmr1 knockout mice behave abnormally and their excitability is higher than that of wild type mice.