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Maternal separation induces long-term oxidative stress alterations and increases anxiety-like behavior of male Balb/cJ mice

Early life stress (ELS) exposure is a well-known risk factor for the development of psychiatric conditions, including anxiety disorder. Preclinical studies show that maternal separation (MS), a classical model of ELS, causes hypothalamic–pituitary–adrenal (HPA) axis alterations, a key contributor to...

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Bibliographic Details
Published in:Experimental brain research 2020-09, Vol.238 (9), p.2097-2107
Main Authors: Malcon, Luiza Martins Costa, Wearick-Silva, Luis Eduardo, Zaparte, Aline, Orso, Rodrigo, Luft, Carolina, Tractenberg, Saulo Gantes, Donadio, Márcio Vinicius Fagundes, de Oliveira, Jarbas Rodrigues, Grassi-Oliveira, Rodrigo
Format: Article
Language:English
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Summary:Early life stress (ELS) exposure is a well-known risk factor for the development of psychiatric conditions, including anxiety disorder. Preclinical studies show that maternal separation (MS), a classical model of ELS, causes hypothalamic–pituitary–adrenal (HPA) axis alterations, a key contributor to the stress response modulation. Given that HPA axis activation has been shown to induce oxidative stress, it is possible to hypothesize that oxidative stress mediates the relationship between chronic ELS exposure and the development of several disorders. Here, we investigate the effects of MS in the oxidative status [plasma and brain reduced glutathione, catalase and thiobarbituric acid reactive substances (TBARS)], metabolism (glucose, triglycerides and cholesterol) and anxiety-like behaviors in adult Balb/cJ mice. In short, we found that MS increased anxiety-like behaviors in the open field, light/dark test but not in the elevated-plus maze. Animals also presented increased circulating cholesterol, increased TBARS in the plasma and decreased catalase in the hippocampus. Our findings suggest that MS induces long-term alterations in oxidative stress and increased anxiety-like behaviors.
ISSN:0014-4819
1432-1106
DOI:10.1007/s00221-020-05859-y