Wang Xiaohong, Xu Jinye, Wang Qing, Ding Dongyi, Wu Lei, Li Ying, Wu Chenghao, Meng Haiwei
School of Medicine, Yangzhou University, Yangzhou, China; Jiangsu Key Laboratory of Experimental & Translational Non-coding RNA Research Noncoding RNA Center, Yangzhou University, YangZhou, 225001, China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, 225009, China; Research Center for Sectional and Imaging Anatomy, Shandong University School of Medicine, Jinan, 250012, China.
School of Medicine, Yangzhou University, Yangzhou, China.
Behav Brain Res. 2021 Feb 5;399:112816. doi: 10.1016/j.bbr.2020.112816. Epub 2020 Aug 9.
Depression occurs in around 40 % of patients with Parkinson's disease (PD) and contributes to severe disability and a poor quality of life. The underlying mechanisms and pathophysiology of depression in PD (PDD) remain obscure, due to a lack of stable animal models of PDD. In this study, we established a PDD model by inducing exposure to chronic mild (CMS) and strong stress (CSS) using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in PD mice. We detected changes in motor and non-motor symptoms, brain structure, neurotransmitters, levels of 5-HT related genes and inflammation. CMS exposed PD (PDMS) mice exhibited obviously decreased levels of neuromuscular strength and enhanced levels of inflammation, compared with that of control mice. CSS exposed MPTP (PDSS) mice exhibited the highest level of motor impairment and depression states along with the highest levels of inflammation enhancement and a decrease in the expression levels of 5-hydroxytryptamine (5-HT) related genes in all groups. Our results suggested that CSS can successfully induce stable depression like symptoms in sub-chronic MPTP PD mice and appears to be a valuable tool for investigating PDD. Furthermore, it was found that 5-HT system dysfunction may contribute to depression like symptoms in PD.
约40%的帕金森病(PD)患者会出现抑郁,这会导致严重残疾和生活质量下降。由于缺乏稳定的帕金森病伴抑郁(PDD)动物模型,PDD的潜在机制和病理生理学仍不清楚。在本研究中,我们通过在PD小鼠中使用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导慢性轻度应激(CMS)和强烈应激(CSS)暴露,建立了PDD模型。我们检测了运动和非运动症状、脑结构、神经递质、5-羟色胺(5-HT)相关基因水平和炎症的变化。与对照小鼠相比,暴露于CMS的PD(PDMS)小鼠的神经肌肉力量水平明显降低,炎症水平升高。暴露于CSS的MPTP(PDSS)小鼠在所有组中表现出最高水平的运动障碍和抑郁状态,同时炎症增强水平最高,5-羟色胺(5-HT)相关基因的表达水平降低。我们的结果表明,CSS可以成功地在亚慢性MPTP诱导的PD小鼠中诱导出稳定的类似抑郁的症状,似乎是研究PDD的一个有价值的工具。此外,还发现5-HT系统功能障碍可能导致PD中类似抑郁的症状。