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目的研究脆性X智力低下蛋白(FMRP)缺失对感觉皮质功能柱神经可塑性的影响。方法从纯合子鼠血液提取DNA,对FMR1基因片段进行扩增,电泳观察结果。并选用子代幼龄FMR1基因敲除及野生型小鼠共16只,按基因型和年龄分为1周龄FMR1基因敲除型组(KO1),1周龄野生型组(WT1),4周龄FMR1基因敲除型组(KO4),4周龄野生型组(WT4),每组各4只。采用快速Golgi染色法分别观察不同发育时间段感觉皮质功能柱区域神经元的功能柱中心和周边两个方向上树突分支、树突棘密度和长度。结果与对照组相比,幼龄FMR1基因敲除鼠树突棘密度显著增高(P<0.05)而长度无变化,感觉皮质功能柱区域中心朝向的树突棘密度无显著性差异,而周边朝向的树突棘密度KO1、KO4分别高于WT1、WT4,并且主要表现在距胞体10～80μm段的密度异常(P<0.01)。结论FMRP缺失导致树突棘密度增高和感觉皮质功能柱区域树突棘修剪异常,并且树突棘修剪和树突修剪的机制不同。
Objective To investigate the effect of fragile X mental retardation protein (FMRP) on the plasticity of sensory cortex neurons. Methods DNA was extracted from the blood of homozygous rats and the FMR1 gene fragment was amplified. The electrophoresis results were observed. A total of 16 young FMR1 knockout and wild type mice were selected and divided into 1 week old FMR1 knockout group (KO1), 1 week old wild type (WT1), 4 Week-old FMR1 knock-out group (KO4), 4-week-old wild-type group (WT4), 4 in each group. The rapid Golgi staining method was used to observe the dendritic branch, density and length of dendritic spines in the center and periphery of the functional column of sensory cortical functional neurons at different developmental stages. Results Compared with the control group, the density of dendritic spines in young FMR1 knockout mice was significantly increased (P <0.05), while the length of dendritic spines did not change. There was no significant difference in the density of dendritic spines between the center of sensory cortex function column and the periphery The densities of dendritic spines KO1 and KO4 were higher than those of WT1 and WT4, respectively, and the densities of dendritic spine were mainly in the range of 10-80 μm (P <0.01). Conclusion The lack of FMRP leads to abnormal densification of dendritic spines and pruning of dendritic spines in the functional cortex of sensory cortex, and the mechanism of dendritic spine pruning and dendritic pruning are different.