Interleukin-1 beta simultaneously affects the stress and reproductive axes by modulating norepinephrine levels in different brain areas

LIFE SCIENCES

卷:91

Article

MohanKumar, P. S.^2,3  MohanKumar, Sheba M. J.¹ 

[1] Michigan State Univ, Dept Pharmacol & Toxicol, Comparat Med & Integrat Biol Program, E Lansing, MI 48824 USA

[2] Michigan State Univ, Dept Pathobiol, E Lansing, MI 48824 USA

[3] Michigan State Univ, Dept Diagnost Invest, E Lansing, MI 48824 USA

关键词: Norepinephrine;    Luteinizing hormone;    Corticosterone;    Stress axis;    Reproductive axis;   

DOI  :  10.1016/j.lfs.2012.09.004

来源: Elsevier

【 摘 要 】

Aims: Interleukin-1 beta (IL-1 beta) is a cytokine that is known to activate the stress axis and suppress the reproductive axis. Different brain areas are involved in the regulation of these two axes. However, they are both under the stimulatory control of the catecholamine, norepinephrine (NE). Here, we hypothesized that IL-1 beta differentially affects these two axes by modulating NE levels in specific brain regions. Main methods: Female Sprague-Dawley rats in proestrus were injected intraperitoneally with either PBS-1.0% BSA (control) or 5 mu g of IL-1 beta at 1 pm. Groups of rats were sacrificed at 1, 3, and 5 pm and their brains were collected. Brain areas associated with reproduction as well as areas associated with stress axis activity were isolated and analyzed for NE concentrations using HPLC-EC. Trunk blood was analyzed for IL-1 beta, corticosterone and luteinizing hormone levels. Key findings: As a general trend, treatment with IL-1 beta significantly decreased NE levels (p<0.05) in the areas controlling reproductive functions when compared to the control group. In contrast, NE levels increased significantly (p<0.05) in the stress associated areas. LH levels were markedly decreased with IL-1 beta treatment while corticosterone levels increased dramatically. Significance: The ability of IL-1 beta to produce differential effects on the stress and reproductive axis could be explained by modulation of NE levels in specific brain areas that are associated with these functions. This differential regulation of NE may be an adaptive phenomenon in response to a systemic immune challenge. (C) 2012 Elsevier Inc. All rights reserved.

【 授权许可】

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