微生物重组可逆转母体饮食引起的后代社会和突触缺陷
Shelly A Buffington1, Gonzalo Viana Di Prisco1, Thomas A Auchtung2
1Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA; Memory and Brain Research Center, Baylor College of Medicine, Houston, TX 77030, USA.
Cell
|June 18, 2016
概括
母亲的高脂肪饮食会改变肠道微生物, 损害后代的社会行为和大脑可塑性. 一种特定的益生菌菌株恢复了小鼠模型中的社会功能和神经生物学.
科学领域:
- 神经科学
- 微生物学
- 发育生物学
背景情况:
- 孕产妇的肥胖与后代的神经发育障碍有关.
- 怀孕期间的饮食因素会影响后代的神经发育.
研究的目的:
- 研究母亲高脂肪饮食对后代社会行为和神经生物学的影响.
- 确定肠道微生物群在这些影响中的作用.
- 探索潜在的治疗干预措施.
主要方法:
- 使用母体高脂肪饮食 (MHFD) 和正常饮食 (MRD) 的小鼠模型.
- 采用共同住房实验和没有细菌的小鼠殖民.
- 评估了社会行为,肠道微生物组成,腹膜区域的突触可塑性 (LTP) 和催产素水平.
- 进行了基因组分析和精确的微生物组复制.
主要成果:
- 在后代中诱导社会缺陷和肠道失调,这些是可转移的.
- 在MHFD后代中,社交互动未能诱导LTP,后代也显示下丘脑氧化素降低.
- 一种单一的细菌菌株纠正了MHFD后代的催产素水平,VTA LTP和社会行为.
结论:
- 母亲饮食引起的肠道微生物不平衡与后代的社会行为和静脉动脉系统的可塑性有因果关系.
- 针对肠道微生物群,可能通过益生菌,可能为神经发育障碍提供治疗策略.
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