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Subchronic Arsenic Exposure Induces Anxiety-Like Behaviors in Normal Mice and Enhances Depression-Like Behaviors in the Chemically Induced Mouse Model of Depression

机译:亚慢性砷暴露在正常小鼠中诱发焦虑样行为并在化学诱导的抑郁症小鼠模型中增强抑郁样行为。

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摘要

Accumulating evidence implicates that subchronic arsenic exposure causes cerebral neurodegeneration leading to behavioral disturbances relevant to psychiatric disorders. However, there is still little information regarding the influence of subchronic exposure to arsenic-contaminated drinking water on mood disorders and its underlying mechanisms in the cerebral prefrontal cortex. The aim of this study is to assess the effects of subchronic arsenic exposure (10 mg/LAs2O3 in drinking water) on the anxiety- and depression-like behaviors in normal mice and in the chemically induced mouse model of depression by reserpine pretreatment. Our findings demonstrated that 4 weeks of arsenic exposure enhance anxiety-like behaviors on elevated plus maze (EPM) and open field test (OFT) in normal mice, and 8 weeks of arsenic exposure augment depression-like behaviors on tail suspension test (TST) and forced swimming test (FST) in the reserpine pretreated mice. In summary, in this present study, we demonstrated that subchronic arsenic exposure induces only the anxiety-like behaviors in normal mice and enhances the depression-like behaviors in the reserpine induced mouse model of depression, in which the cerebral prefrontal cortex BDNF-TrkB signaling pathway is involved. We also found that eight weeks of subchronic arsenic exposure are needed to enhance the depression-like behaviors in the mouse model of depression. These findings imply that arsenic could be an enhancer of depressive symptoms for those patients who already had the attribute of depression.
机译:越来越多的证据表明,亚慢性砷暴露会导致脑神经变性,从而导致与精神疾病有关的行为障碍。但是,关于亚慢性暴露于砷污染的饮用水对情绪障碍及其在大脑前额叶皮层中的潜在机制的影响,目前尚无足够的信息。这项研究的目的是评估亚慢性砷暴露(饮用水中10μmg/ LAs2O3)对利血平预处理的正常小鼠和化学诱导的小鼠抑郁模型中焦虑和抑郁样行为的影响。我们的发现表明,在正常小鼠中,砷暴露4周可增强高迷宫(EPM)和开放视野测试(OFT)的焦虑样行为,而砷暴露8周可增强尾部悬吊测试(TST)的抑郁样行为利血平预处理的小鼠进行强制游泳测试(FST)。总之,在本研究中,我们证明了亚慢性砷暴露仅在正常小鼠中诱发焦虑样行为,并在利血平诱发的抑郁症小鼠模型中增强了抑郁样行为,其中脑前额叶皮层BDNF-TrkB信号传导涉及途径。我们还发现,需要八周的亚慢性砷暴露来增强抑郁症小鼠模型中的抑郁症样行为。这些发现表明,对于那些已经患有抑郁症的患者,砷可能是抑郁症状的增强剂。

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