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早年逆境或高脂肪饮食摄入会降低成年大鼠的认知功能并改变脑源性神经营养因子(BDNF)信号传导:这些因素的相互作用会改变这些影响。

Early life adversities or high fat diet intake reduce cognitive function and alter BDNF signaling in adult rats: Interplay of these factors changes these effects.

作者信息

Arcego Danusa Mar, Krolow Rachel, Lampert Carine, Toniazzo Ana Paula, Berlitz Carolina, Lazzaretti Camilla, Schmitz Felipe, Rodrigues André Felipe, Wyse Angela T S, Dalmaz Carla

机构信息

Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, UFRGS, Porto Alegre, Rio Grande do Sul, Brazil.

Programa de Pós-Graduação em Saúde e Comportamento, Universidade Católica de Pelotas (UCPel), Pelotas, RS, Brazil.

出版信息

Int J Dev Neurosci. 2016 May;50:16-25. doi: 10.1016/j.ijdevneu.2016.03.001. Epub 2016 Mar 4.

DOI:10.1016/j.ijdevneu.2016.03.001
PMID:26948152
Abstract

Environmental factors, like early exposure to stressors or high caloric diets, can alter the early programming of central nervous system, leading to long-term effects on cognitive function, increased vulnerability to cognitive decline and development of psychopathologies later in life. The interaction between these factors and their combined effects on brain structure and function are still not completely understood. In this study, we evaluated long-term effects of social isolation in the prepubertal period, with or without chronic high fat diet access, on memory and on neurochemical markers in the prefrontal cortex of rats. We observed that early social isolation led to impairment in short-term and working memory in adulthood, and to reductions of Na(+),K(+)-ATPase activity and the immunocontent of phospho-AKT, in prefrontal cortex. Chronic exposure to a high fat diet impaired short-term memory (object recognition), and decreased BDNF levels in that same brain area. Remarkably, the association of social isolation with chronic high fat diet rescued the memory impairment on the object recognition test, as well as the changes in BDNF levels, Na(+),K(+)-ATPase activity, MAPK, AKT and phospho-AKT to levels similar to the control-chow group. In summary, these findings showed that a brief social isolation period and access to a high fat diet during a sensitive developmental period might cause memory deficits in adulthood. On the other hand, the interplay between isolation and high fat diet access caused a different brain programming, preventing some of the effects observed when these factors are separately applied.

摘要

环境因素,如早期暴露于应激源或高热量饮食,可改变中枢神经系统的早期编程,导致对认知功能的长期影响,增加晚年认知衰退和精神病理学发展的易感性。这些因素之间的相互作用及其对脑结构和功能的综合影响仍未完全了解。在本研究中,我们评估了青春期前社会隔离(无论是否可长期获取高脂饮食)对大鼠记忆及前额叶皮质神经化学标志物的长期影响。我们观察到,早期社会隔离导致成年大鼠短期和工作记忆受损,前额叶皮质中Na(+)、K(+)-ATP酶活性及磷酸化AKT免疫含量降低。长期暴露于高脂饮食会损害短期记忆(物体识别),并降低同一脑区的脑源性神经营养因子(BDNF)水平。值得注意的是,社会隔离与长期高脂饮食相结合可挽救物体识别测试中的记忆损伤,以及BDNF水平、Na(+)、K(+)-ATP酶活性、丝裂原活化蛋白激酶(MAPK)、AKT和磷酸化AKT的变化,使其恢复至与对照组相似的水平。总之,这些发现表明,在敏感发育时期的短暂社会隔离期及获取高脂饮食可能会导致成年期记忆缺陷。另一方面,隔离与高脂饮食之间的相互作用导致了不同的脑编程,防止了单独应用这些因素时所观察到的一些影响。

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