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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Enriched environment promotes behavioral and morphological recovery in a mouse model for the fragile X syndrome
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Enriched environment promotes behavioral and morphological recovery in a mouse model for the fragile X syndrome

机译：丰富的环境促进脆弱X综合征的小鼠模型的行为和形态恢复

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摘要

Fragile X syndrome, the most frequent form of hereditary mental retardation, is due to a mutation of the fragile X mental retardation 1 (FMR1) gene on the X chromosome. Like fragile X patients, FMR1-knockout (FMR1-KO) mice lack the normal fragile X mental retardation protein (FMRP) and show both cognitive alterations and an immature neuronal morphology. We reared FMR1-KO mice in a C57BL/6 background in enriched environmental conditions to examine the possibility that experience-dependent stimulation alleviates their behavioral and neuronal abnormalities. FMR1-KO mice kept in standard cages were hyperactive, displayed an altered pattern of open field exploration, and did not show habituation. Quantitative morphological analyses revealed a reduction in basal dendrite length and branching together with more immature-appearing spines along apical dendrites of layer five pyramidal neurons in the visual cortex. Enrichment largely rescued these behavioral and neuronal abnormalities while increasing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor subunit 1 (GluR1) levels in both genotypes. Enrichment did not, however, affect FMRP levels in the WT mice. These data suggest that FMRP-independent pathways activating glutamatergic signaling are preserved in FMR1-KO mice and that they can be elicited by environmental stimulation.
机译：脆性X综合征是遗传性智力低下的最常见形式，是由于X染色体上的脆性X智力低下1（FMR1）基因的突变引起的。像脆弱的X患者一样，FMR1基因敲除（FMR1-KO）小鼠缺乏正常的脆弱X智力障碍蛋白（FMRP），并且显示出认知改变和不成熟的神经元形态。我们在丰富的环境条件下将FMR1-KO小鼠饲养在C57BL / 6背景下，以检查依赖于经验的刺激减轻其行为和神经元异常的可能性。饲养在标准笼子中的FMR1-KO小鼠活动过度，表现出改变的野外探索模式，并且没有表现出习惯性。定量的形态学分析显示，沿着视觉皮层中第5层锥体神经元的顶端树突，基底树突长度减少，分支增加，同时出现更多未成熟的棘突。富集主要挽救了这些行为和神经元异常，同时增加了两种基因型的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）谷氨酸受体亚基1（GluR1）的水平。但是，富集并不影响野生型小鼠的FMRP水平。这些数据表明，在FMR1-KO小鼠体内保留了激活FMRP的途径，它们不依赖于FMRP激活谷氨酸能信号传导，并且可以通过环境刺激来诱导它们。

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