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Combined exposure to maternal high-fat diet and neonatal lipopolysaccharide disrupts stress-related signaling but normalizes spatial memory in juvenile rats
Brain, Behavior, and Immunity ( IF 8.8 ) Pub Date : 2022-03-05 , DOI: 10.1016/j.bbi.2022.03.003
Mouly F Rahman 1 , Ceren B Yuksel 2 , Patrick O McGowan 3
Affiliation  

Both neonatal infections and exposure to maternal obesity are inflammatory stressors in early life linked to increased rates of psychopathologies related to mood and cognition. Epidemiological studies indicate that neonates born to mothers with obesity have a higher likelihood of developing neonatal infections, however effects on offspring physiology and behavior resulting from the combination of these stressors have yet to be investigated. The aim of this study was to explore immediate and persistent phenotypes resulting from neonatal lipopolysaccharide (nLPS) administration in rat offspring born to dams consuming a high-fat diet (HFD). Neural transcript abundance of genes involved with stress regulation and spatial memory were examined alongside related behaviors. At the juvenile age point, unlike offspring exposed to maternal HFD (mHFD) or nLPS alone, offspring with combined exposure to mHFD + nLPS displayed altered transcript abundances of stress-related genes in the ventral hippocampus (HPC) in a manner conducive to potentiating stress responses. For memory-related phenotypes, juveniles exposed to mHFD + nLPS exhibited normalized spatial memory and levels of memory-related gene expression in the dorsal HPC similar to control diet offspring, while control diet + nLPS, and mHFD offspring exhibited reduced levels of memory-related gene expression and impaired spatial memory. These findings suggest that dual exposure to unique inflammatory stressors in early life can disrupt neural stress regulation but normalize spatial memory processes.



中文翻译:

母体高脂肪饮食和新生儿脂多糖的联合暴露破坏了与压力相关的信号传导,但使幼年大鼠的空间记忆正常化

新生儿感染和暴露于孕产妇肥胖都是生命早期的炎症压力源,与情绪和认知相关的精神病理学发病率增加有关。流行病学研究表明,肥胖母亲所生的新生儿发生新生儿感染的可能性更高,但这些压力源的组合对后代生理和行为的影响尚待研究。本研究的目的是探索在食用高脂饮食 (HFD) 的大坝所生的大鼠后代中,由新生儿脂多糖 (nLPS) 给药产生的即时和持久表型。与相关行为一起检查了与压力调节和空间记忆有关的基因的神经转录本丰度。在少年时代,与单独暴露于母体 HFD (mHFD) 或 nLPS 的后代不同,同时暴露于 mHFD + nLPS 的后代以有利于增强应激反应的方式显示腹侧海马 (HPC) 中应激相关基因的转录丰度改变。对于记忆相关表型,暴露于 mHFD + nLPS 的青少年在背侧 HPC 中表现出标准化的空间记忆和记忆相关基因表达水平,与对照饮食后代相似,而对照饮食 + nLPS 和 mHFD 后代表现出与记忆相关的水平降低基因表达和空间记忆受损。这些发现表明,在生命早期双重暴露于独特的炎症压力源会破坏神经压力调节,但会使空间记忆过程正常化。联合暴露于 mHFD + nLPS 的后代以有利于增强应激反应的方式显示腹侧海马 (HPC) 中应激相关基因的转录丰度改变。对于记忆相关表型,暴露于 mHFD + nLPS 的青少年在背侧 HPC 中表现出标准化的空间记忆和记忆相关基因表达水平,与对照饮食后代相似,而对照饮食 + nLPS 和 mHFD 后代表现出与记忆相关的水平降低基因表达和空间记忆受损。这些发现表明,在生命早期双重暴露于独特的炎症压力源会破坏神经压力调节,但会使空间记忆过程正常化。联合暴露于 mHFD + nLPS 的后代以有利于增强应激反应的方式显示腹侧海马 (HPC) 中应激相关基因的转录丰度改变。对于记忆相关表型,暴露于 mHFD + nLPS 的青少年在背侧 HPC 中表现出标准化的空间记忆和记忆相关基因表达水平,与对照饮食后代相似,而对照饮食 + nLPS 和 mHFD 后代表现出与记忆相关的水平降低基因表达和空间记忆受损。这些发现表明,在生命早期双重暴露于独特的炎症压力源会破坏神经压力调节,但会使空间记忆过程正常化。暴露于 mHFD + nLPS 的青少年在背部 HPC 中表现出标准化的空间记忆和记忆相关基因表达水平,与对照饮食后代相似,而对照饮食 + nLPS 和 mHFD 后代表现出记忆相关基因表达水平降低和空间记忆受损. 这些发现表明,在生命早期双重暴露于独特的炎症压力源会破坏神经压力调节,但会使空间记忆过程正常化。暴露于 mHFD + nLPS 的青少年在背部 HPC 中表现出标准化的空间记忆和记忆相关基因表达水平,与对照饮食后代相似,而对照饮食 + nLPS 和 mHFD 后代表现出记忆相关基因表达水平降低和空间记忆受损. 这些发现表明,在生命早期双重暴露于独特的炎症压力源会破坏神经压力调节,但会使空间记忆过程正常化。

更新日期:2022-03-05
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