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盐作为一种无热量的行为调节剂:来自临床前研究的证据综述。

Salt as a non-caloric behavioral modifier: A review of evidence from pre-clinical studies.

机构信息

Department of Psychological Sciences & Brain Health Research Institute, Kent State University, Kent, OH, 44242, USA.

出版信息

Neurosci Biobehav Rev. 2022 Apr;135:104385. doi: 10.1016/j.neubiorev.2021.10.007. Epub 2021 Oct 8.

DOI:10.1016/j.neubiorev.2021.10.007
PMID:34634356
Abstract

Though excess salt intake is well-accepted as a dietary risk factor for cardiovascular diseases, relatively little has been explored about how it impacts behavior, despite the ubiquity of salt in modern diets. Given the challenges of manipulating salt intake in humans, non-human animals provide a more tractable means for evaluating behavioral sequelae of high salt. By describing what is known about the impact of elevated salt on behavior, this review highlights how underexplored salt's behavioral effects are. Increased salt consumption in adulthood does not affect spontaneous anxiety-related behaviors or locomotor activity, nor acquisition of maze or fear tasks, but does impede expression of spatial/navigational and fear memory. Nest building is reduced by heightened salt in adults, and stress responsivity is augmented. When excess salt exposure occurs during development, and/or to parents, offspring locomotion is increased, and both spatial memory expression and social investigation are attenuated. The largely consistent findings reviewed here indicate expanded study of salt's effects will likely uncover broader behavioral implications, particularly in the scarcely studied female sex.

摘要

尽管过量摄入盐被认为是心血管疾病的饮食风险因素,但尽管现代饮食中普遍存在盐,人们对盐如何影响行为的研究相对较少。鉴于人类控制盐摄入量的挑战,非人类动物为评估高盐对行为的后续影响提供了一种更易于处理的方法。本文通过描述已知的盐对行为的影响,强调了盐对行为影响的研究还很不足。成年期盐摄入量增加不会影响与焦虑相关的自发行为或运动活动,也不会影响迷宫或恐惧任务的获得,但会阻碍空间/导航和恐惧记忆的表达。筑巢行为在成年期因盐含量增加而减少,应激反应增强。当过量的盐暴露发生在发育期间和/或在父母身上时,后代的运动增加,空间记忆表达和社会探索都减弱。本文综述的一致性研究结果表明,对盐的影响进行更广泛的研究可能会揭示更广泛的行为影响,特别是在研究甚少的女性中。

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High salt intake activates the hypothalamic-pituitary-adrenal axis, amplifies the stress response, and alters tissue glucocorticoid exposure in mice.
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