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Aldosterone synergizes with peripheral inflammation to induce brain IL-1[beta] expression and depressive-like effects

Recent findings have shown that the physiological functions of the hormone aldosterone go far beyond its well-known role in blood-pressure regulation and salt/water homeostasis. Aldosterone is for example involved in the regulation of inflammation, and also binds directly to mineralocorticoid recept...

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Bibliographic Details
Published in:Cytokine (Philadelphia, Pa.) Pa.), 2012-12, Vol.60 (3), p.749-754
Main Authors: Bay-Richter, Cecilie, Hallberg, Ludvig, Ventorp, Filip, Janelidze, Shorena, Brundin, Lena
Format: Article
Language:English
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Summary:Recent findings have shown that the physiological functions of the hormone aldosterone go far beyond its well-known role in blood-pressure regulation and salt/water homeostasis. Aldosterone is for example involved in the regulation of inflammation, and also binds directly to mineralocorticoid receptors in specific brain regions. Interestingly, depressive symptoms appear to correlate with alterations of the aldosterone system but the underlying mechanisms have not been elucidated. In this study aldosterone (2 mu g/100 g body weight/day) was continuously administered via osmotic minipumps for 5 days. Lipopolysaccharide (LPS) was administered once a day for 5 days in a dose of 1 mg/kg ip. The rats were tested for depressive-like behavior 24 h after the last LPS injection. Protein levels of cytokines were measured in serum and cerebrospinal fluid (CSF). mRNA expression of interleukin (IL)-1[beta] and IL-6 in the prefrontal cortex (PFC) was analyzed using reverse transcriptase qPCR. We found that aldosterone treatment increased LPS-induced IL-1[beta] mRNA expression in the PFC and CSF. Moreover, there was a positive correlation between IL-1[beta] in CSF and depressive-like behaviors. These findings suggest that IL-1[beta] is affected by the reninaaldosteroneaangiotensin system (RAAS) activity and connected to symptoms of depression.
ISSN:1043-4666
DOI:10.1016/j.cyto.2012.08.016