Major depressive disorder mediates accelerated aging in rats subjected to chronic mild stress

Xie, Xiaoxian; Chen, Yangyang; Ma, Lingyan; Shen, Qichen; Huang, Liangfeng; Zhao, Binggong; Wu, Tao; Fu, Zhengwei

doi:10.1016/j.bbr.2017.04.022

Cited by 38 publications

(15 citation statements)

References 57 publications

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“…Superoxide is a precursor for ROS, and complex I and III are mainly responsible for its production ( Vakifahmetoglu-Norberg et al, 2017 ). Oxidative stress could be the cause or consequence of damage to mitochondria and mtDNA ( Xie et al, 2017 ). Martins-de-Souza et al (2012) speculated that a reduction in ATP could be due to oxidative stress and that the increased levels of subunits of OXPHOS complexes were compensatory.…”

Section: Oxidative Stressmentioning

confidence: 99%

Mitochondria and Mood: Mitochondrial Dysfunction as a Key Player in the Manifestation of Depression

et al. 2018

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Human and animal studies suggest an intriguing link between mitochondrial diseases and depression. Although depression has historically been linked to alterations in monoaminergic pharmacology and adult hippocampal neurogenesis, new data increasingly implicate broader forms of dampened plasticity, including plasticity within the cell. Mitochondria are the cellular powerhouse of eukaryotic cells, and they also regulate brain function through oxidative stress and apoptosis. In this paper, we make the case that mitochondrial dysfunction could play an important role in the pathophysiology of depression. Alterations in mitochondrial functions such as oxidative phosphorylation (OXPHOS) and membrane polarity, which increase oxidative stress and apoptosis, may precede the development of depressive symptoms. However, the data in relation to antidepressant drug effects are contradictory: some studies reveal they have no effect on mitochondrial function or even potentiate dysfunction, whereas other studies show more beneficial effects. Overall, the data suggest an intriguing link between mitochondrial function and depression that warrants further investigation. Mitochondria could be targeted in the development of novel antidepressant drugs, and specific forms of mitochondrial dysfunction could be identified as biomarkers to personalize treatment and aid in early diagnosis by differentiating between disorders with overlapping symptoms.

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Section: Oxidative Stressmentioning

confidence: 99%

Mitochondria and Mood: Mitochondrial Dysfunction as a Key Player in the Manifestation of Depression

et al. 2018

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“…In an attempt to better position their ostensible stress hyporesponsiveness in its relevant (patho)physiological context (i.e., resilience as opposed to cognitive-emotional deficit), we exposed Ahi1+/− mice to a protocol of chronic unpredictable stress (CUS) that consisted of various psychological stressors administered in random order over a period of 9 weeks. CUS paradigms are based on the chronic, mild stress protocol of Willner et al 20 that has been shown to induce anhedonia (e.g., 21 , 22 ) along with decreased hippocampal neurogenesis 23 , 24 . With respect to anxiety, data are less consistent.…”

Section: Introductionmentioning

confidence: 99%

Effect of chronic unpredictable stress on mice with developmental under-expression of the Ahi1 gene: behavioral manifestations and neurobiological correlates

et al. 2018

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The Abelson helper integration site 1 (Ahi1) gene plays a pivotal role in brain development and is associated with genetic susceptibility to schizophrenia, and other neuropsychiatric disorders. Translational research in genetically modified mice may reveal the neurobiological mechanisms of such associations. Previous studies of mice heterozygous for Ahi1 knockout (Ahi1+/−) revealed an attenuated anxiety response on various relevant paradigms, in the context of a normal glucocorticoid response to caffeine and pentylenetetrazole. Resting-state fMRI showed decreased amygdalar connectivity with various limbic brain regions and altered network topology. However, it was not clear from previous studies whether stress-hyporesponsiveness reflected resilience or, conversely, a cognitive-emotional deficit. The present studies were designed to investigate the response of Ahi1+/− mice to chronic unpredictable stress (CUS) applied over 9 weeks. Wild type (Ahi1+/+) mice were significantly affected by CUS, manifesting decreased sucrose preference (p < 0.05); reduced anxiety on the elevated plus maze and light dark box and decreased thigmotaxis in the open field (p < 0.01 0.05); decreased hyperthermic response to acute stress (p < 0.05); attenuated contextual fear conditioning (p < 0.01) and increased neurogenesis (p < 0.05). In contrast, Ahi1+/− mice were indifferent to the effects of CUS assessed with the same parameters. Our findings suggest that Ahi1 under-expression during neurodevelopment, as manifested by Ahi1+/− mice, renders these mice stress hyporesponsive. Ahi1 deficiency during development may attenuate the perception and/or integration of environmental stressors as a result of impaired corticolimbic connectivity or aberrant functional wiring. These neural mechanisms may provide initial clues as to the role Ahi1 in schizophrenia and other neuropsychiatric disorders.

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“…Remarkably, EAP mice also displayed a decrease in total travel distance, which was suggestive of hypolocomotion, albeit it did not reach statistical significance (Figure S1). It has been reported in other animal models of depression that stress and inflammation may decrease the locomotoractivity of rodents 34,35 . Hence, we speculated that the hypolocomotion of EAP mice in this study was potentially due to EAP‐related stress and immune inflammation.…”

Section: Discussionmentioning

confidence: 65%

Abnormal gut microbiota composition is associated with experimental autoimmune prostatitis‐induced depressive‐like behaviors in mice

Liu

Zhang

et al. 2020

The Prostate

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Background: Depressive symptoms are found in approximately 78% of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) patients, but the pathological mechanisms remain unknown. Increasing evidence suggests that abnormal gut microbiota may play an important role in depression. Thus, we aimed to investigate whether gut microbiota contributes to CP/CPPS-associated depression by using a mouse model of experimental autoimmune prostatitis (EAP).Methods: Male nonobese diabetic mice were immunized twice by subcutaneous injection of prostate antigen and adjuvant. Behavioral tests consisted of an open field test, sucrose preference test, forced swimming tests, and tail suspension test was used to confirm the depression-like symptoms that were induced by EAP. Then, fecal samples were collected, and 16S ribosomal RNA gene sequencing was performed to detect differences in gut microbiota composition between control and EAP group. Additionally, fecal bacteria from the control and EAP mice were transplanted into antibiotics-induced pseudo-germ-free mice to investigate the effects on host behaviors and the composition of gut bacteria.Results: EAP was successfully established and exhibited depressive-like behaviors in mice. The 16S rRNA analysis of fecal samples indicated the abnormal composition of gut microbiota in the EAP mice compared to the control mice. In the fecal microbiota transplant study, antibiotics-treated pseudo-germ-free mice presented depressive states as compared to naïve mice. Fecal bacteria transplant from EAP mice, but not from control mice, into the pseudo-germ-free mice, significantly exaggerated host depression-like behaviors. Moreover, fecal bacteria transplants from control and EAP mice induced distinct alterations in α-diversity and β-diversity indices. In all, 24 bacteria at six phylogenetic levels were remarkably changed by the fecal bacteria transplantation.Conclusions: Abnormal gut microbiota composition after EAP induction may contribute to the development of depression in mice. A therapeutic strategy that targets gut microbiota may provide an alternative treatment for alleviating this condition. K E Y W O R D Sdepression, fecal bacteria transplantation, gut microbiota, prostatitis

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Major depressive disorder mediates accelerated aging in rats subjected to chronic mild stress

Cited by 38 publications

References 57 publications

Mitochondria and Mood: Mitochondrial Dysfunction as a Key Player in the Manifestation of Depression

Mitochondria and Mood: Mitochondrial Dysfunction as a Key Player in the Manifestation of Depression

Effect of chronic unpredictable stress on mice with developmental under-expression of the Ahi1 gene: behavioral manifestations and neurobiological correlates

Abnormal gut microbiota composition is associated with experimental autoimmune prostatitis‐induced depressive‐like behaviors in mice

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