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Metabolic syndrome accentuates post-traumatic stress disorder-like symptoms and glial activation.
Behavioural Brain Research ( IF 2.7 ) Pub Date : 2020-02-20 , DOI: 10.1016/j.bbr.2020.112557
Ana Cláudia Alves Freire Ribeiro 1 , Tatiane Helena Batista 1 , Viviana Carolina Trujillo Rojas 1 , Alexandre Giusti-Paiva 1 , Fabiana Cardoso Vilela 1
Affiliation  

The relationship between individuals with post-traumatic stress disorder (PTSD) and the development of metabolic syndrome (MS) is well understood, but the relationship between individuals with preexisting MS and the development of PTSD is not yet known. Therefore, we evaluated the course of PTSD development in preexisting MS rats and we quantified the glial fibrillary acidic protein (GFAP) and ionized the calcium binding adaptor molecule 1 (Iba-1) in the cortex and hippocampus of the experimental animals. Male Wistar rats were divided into two groups: control or 10 % fructose for 5 weeks. After 5 weeks of MS induction, a group of animals was used to characterize MS. In another group, after 5 weeks of MS induction, animals were exposed to or not exposed to inescapable footshocks, followed by social isolation. After 14 days of a retention interval, the animals were re-exposed to the inescapable footshocks box, and the freezing time was evaluated. Over the following days, the animals were tested using the open field, social interaction and forced swimming tests, respectively. In another group of animals, after induction of MS and PTSD as previously described, elevated plus maze and object recognition tests were performed. Our results demonstrate that fructose solution for 5 weeks was able to induce MS, and animals with MS had more pronounced PTSD-like symptoms and a greater increase in GFAP and Iba-1 in the hippocampus and prefrontal cortex. In conclusion, MS accentuated PTSD-like symptoms that may be related to increased glial activation. This study helps reveal factors that may predispose individuals to the development of PTSD, such as metabolic disorders.

中文翻译:

代谢综合症加剧了创伤后应激障碍样症状和神经胶质激活。

患有创伤后应激障碍(PTSD)的个体与代谢综合征(MS)的发展之间的关系已广为人知,但先前患有MS的个体与PTSD的发展之间的关系尚不明确。因此,我们评估了已有MS大鼠的PTSD发育过程,并量化了胶质纤维酸性蛋白(GFAP)并电离了实验动物皮层和海马中的钙结合衔接子分子1(Iba-1)。将雄性Wistar大鼠分成两组:对照组或10%果糖,持续5周。MS诱导5周后,使用一组动物表征MS。在另一组中,MS诱发5周后,使动物暴露于或不暴露于不可避免的足底,然后进行社会隔离。保留间隔14天后,将动物重新暴露于不可避免的脚踩箱中,并评估冷冻时间。在接下来的几天中,分别使用野外测试,社交互动和强迫游泳测试对动物进行了测试。在另一组动物中,如前所述诱导MS和PTSD后,进行高架迷宫和物体识别测试。我们的结果表明,果糖溶液持续5周能够诱导MS,患有MS的动物具有更明显的PTSD样症状,海马和前额叶皮层中的GFAP和Iba-1的增加更大。总之,MS加重了PTSD样症状,这可能与神经胶质激活增加有关。这项研究有助于揭示可能使个体易患PTSD的因素,例如代谢紊乱。
更新日期:2020-02-12
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