Laboratory of Physiology, Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Laboratory of Immunology, Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Brain Behav Immun. 2014 Mar;37:164-76. doi: 10.1016/j.bbi.2013.12.003. Epub 2013 Dec 8.
There is converging evidence that prenatal maternal infection can increase the risk of occurrence of neuropsychiatric disorders like schizophrenia, autism, anxiety and depression in later life. Experimental studies have shown conflicting effects of prenatal maternal immune activation on anxiety-like behavior and hypothalamic-pituitary-adrenal (HPA) axis development in offspring. We investigated the effects of maternal immune activation during pregnancy on anxiety- and depression-like behaviors in pregnant mice and their offspring to determine whether these effects are dependent on strain. NMRI and C57BL/6 pregnant mice were treated with either saline or lipopolysaccharide on gestational day 17 and then interleukin (IL)-6 and corticosterone (COR) levels; anxiety or depression in the pregnant mice and their offspring were evaluated. The results indicate that maternal inflammation increased the levels of COR and anxiety-like behavior in NMRI pregnant mice, but not in C57BL/6 dams. Our data also demonstrate that maternal inflammation elevated the levels of anxiety-and depression-like behaviors in NMRI offspring on the elevated plus-maze, elevated zero-maze, tail suspension test and forced swimming test respectively, but not in the open field and light-dark box. In addition, we did not find any significant change in anxiety- and depression-like behaviors of adult C57BL/6 offspring. Our findings suggest that prenatal maternal immune activation can alter the HPA axis activity, anxiety- and depression-like behaviors in a strain- and task-dependent manner in offspring and further comprehensive studies are needed to prove the causal relationship between the findings found here and to validate their relevance to neuropsychiatric disorders in humans.
越来越多的证据表明，产前母体感染会增加精神神经障碍（如精神分裂症、自闭症、焦虑和抑郁）的发生风险。实验研究表明，产前母体免疫激活对后代焦虑样行为和下丘脑-垂体-肾上腺（HPA）轴发育的影响存在矛盾。我们研究了孕期母体免疫激活对怀孕小鼠及其后代焦虑和抑郁样行为的影响，以确定这些影响是否取决于品系。在妊娠第 17 天，NMRI 和 C57BL/6 孕鼠分别用生理盐水或脂多糖处理，然后检测白细胞介素（IL）-6 和皮质酮（COR）水平；评估孕鼠及其后代的焦虑或抑郁情况。结果表明，母体炎症增加了 NMRI 孕鼠的 COR 和焦虑样行为水平，但对 C57BL/6 孕鼠没有影响。我们的数据还表明，母体炎症使 NMRI 后代在高架十字迷宫、高架零迷宫、悬尾试验和强迫游泳试验中的焦虑和抑郁样行为水平升高，但在旷场和明暗箱中没有升高。此外，我们没有发现成年 C57BL/6 后代的焦虑和抑郁样行为有任何显著变化。我们的研究结果表明，产前母体免疫激活可以以一种依赖于品系和任务的方式改变 HPA 轴活性、焦虑和抑郁样行为，还需要进一步进行全面的研究来证明这里发现的因果关系，并验证它们与人类神经精神障碍的相关性。
