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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Nervous System Deletion of Mammalian INDY in Mice Mimics Dietary Restriction-Induced Memory Enhancement
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Nervous System Deletion of Mammalian INDY in Mice Mimics Dietary Restriction-Induced Memory Enhancement

机译：神经系统缺失哺乳动物Indy在小鼠模仿膳食限制诱导的记忆增强

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Reduced expression of the Indy (I'm Not Dead Yet) gene extends life span in Caenorhabditis elegans and Drosophila melanogaster and improves the metabolic heath of Mus musculus through inducing a physiological status akin to dietary restriction (DR). Although the function of Indy in aging and hepatic metabolism has been extensively studied, its role in the mouse nervous system remains unclear. Here, we explore the effect of mammalian Indy (mIndy, SLC13A5) gene deletion on murine cognitive function. Similar to what is seen in DR animals, systemic deletion of the mIndy gene (mIndy knockout [KO]) significantly improves memory performance and motor coordination of mice. Both DR and mIndy KO mice act normally in other behavioral tasks, including emotional, social, and food-seeking behaviors. Moreover, we find that tissue-specific deletion of mIndy in the nervous system is sufficient to improve memory performance, while liver-specific deletion has no effect on memory, and results in tests of motor coordination show no changes in either mutant. Mice with systemic or nervous system deletion of mIndy also exhibit increased hippocampal neurogenesis and dendritic spine formation in dentate granule cells; these changes are well-documented contributors to enhanced memory performance. Together, our studies demonstrate a critical role for brain-derived mIndy expression in the regulation of memory function in animals.
机译：Indy（我还没死）基因表达的减少延长了秀丽隐杆线虫和黑腹果蝇的寿命，并通过诱导类似于饮食限制（DR）的生理状态改善了小家鼠的代谢健康。虽然Indy在衰老和肝脏代谢中的作用已被广泛研究，但其在小鼠神经系统中的作用仍不清楚。在这里，我们探讨哺乳动物Indy（mIndy，SLC13A5）基因缺失对小鼠认知功能的影响。与DR动物的情况类似，mIndy基因的系统性缺失（mIndy敲除[KO]）显著改善了小鼠的记忆能力和运动协调能力。DR和mIndy KO小鼠在其他行为任务中的行为正常，包括情绪、社交和觅食行为。此外，我们发现，神经系统中mIndy的组织特异性缺失足以改善记忆表现，而肝脏特异性缺失对记忆没有影响，运动协调性测试的结果显示，这两种突变都没有变化。mIndy系统性或神经系统缺失的小鼠在齿状颗粒细胞中也表现出海马神经发生和树突棘形成增加；这些更改是增强内存性能的有据可查的因素。总之，我们的研究证明了脑源性mIndy表达在动物记忆功能调节中的关键作用。

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