The Effects of Stress and Diet on the “Brain–Gut” and “Gut–Brain” Pathways in Animal Models of Stress and Depression

Herselman, Mauritz Frederick; Bailey, Sheree; Bobrovskaya, Larisa

doi:10.3390/ijms23042013

Cited by 25 publications

(19 citation statements)

References 150 publications

(409 reference statements)

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“… 8 Moreover, an unhealthy diet and environmental exposures that influence the gut microbial composition were proved to be highly associated with the increased incidence of depression in recent years. 9 , 10 …”

Section: Introductionmentioning

confidence: 99%

Gut microbiota and its metabolites in depression: from pathogenesis to treatment

Liu¹,

Wang²,

Chen³

et al. 2023

eBioMedicine

185

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Section: Introductionmentioning

confidence: 99%

Gut microbiota and its metabolites in depression: from pathogenesis to treatment

Liu¹,

Wang²,

Chen³

et al. 2023

eBioMedicine

185

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“…Second, on the one hand, decreased levels of 5‐HT and increased 5‐HT turnover in brain are known to be a major pathophysiological mechanism of depression [18, 19]. On the other hand, IDO1, the important molecule related to 5‐HT level in brain [47], its increased level also indicated the decreased synthesis of 5‐HT [27]. All these indicators verify the depressive‐like behaviors in mice, which is consistent with the previous study [46].…”

Section: Discussionmentioning

confidence: 99%

Blocking coprophagy increases the levels of inflammation and depression in healthy mice as well as mice receiving fecal microbiota transplantation from disease model mice donors

Sha

Xiao

Yang

et al. 2023

APMIS

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Blocking coprophagy increases the levels of inflammation and depression in healthy mice as well as mice receiving fecal microbiota transplantation from disease model mice donors. APMIS. 2023; 131: 351-368. Rodents have been extensively used as animal models in microbiome studies. However, all rodents have a habitual nature called coprophagy, a phenomenon that they self-reinoculate feces into their gastrointestinal tract. Recent studies have shown that blocking coprophagy can alter rodents' diversity of gut microbiota, metabolism, neurochemistry, and cognitive behavior. However, whether rodents' coprophagy behavior affects the levels of inflammation and depression is unclear. In order to address this problem, we first blocked coprophagy in healthy mice. It displayed an increase in the levels of depression, verified by depressive-like behaviors and mood-related indicators, and inflammation, verified by the increased levels of the pro-inflammatory cytokine, in coprophagy-blocked mice. Furthermore, we transplanted fecal microbiota from chronic restraint stress (CRS) depression model mice and lipopolysaccharide (LPS) inflammation model mice to healthy recipient mice, respectively. It showed that the disease-like phenotypes in the coprophagyblocked group were worse than those in the coprophagy-unblocked group, including severer depressive symptoms and higher levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α and IFN-γ) in serum, prefrontal cortex (PFC), and hippocampus (HIP). These findings showed that blocking coprophagy in mice not only increased the levels of inflammation and depression in healthy mice but also aggravated inflammation and depression induced by fecal microbiota from disease donors. The discovery may provide a vital reference for future research involving FMT in rodents.

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“…Finally, the gut microbiome and gut-brain axis are key players in stress related diseases including cardiovascular, metabolic and mood disorders (296-298), and are sex-dependent and sensitive to gonadal hormones (299)(300)(301)(302)(303)(304). Indeed, an oestrogen-gut microbiome axis is implicated in sex and oestrogen sensitive chronic disease (305).…”

Section: Gut Biology and Microbiomementioning

confidence: 99%

The sex-dependent response to psychosocial stress and ischaemic heart disease

Helman

Headrick

Stapelberg

et al. 2023

Front. Cardiovasc. Med.

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Stress is an important risk factor for modern chronic diseases, with distinct influences in males and females. The sex specificity of the mammalian stress response contributes to the sex-dependent development and impacts of coronary artery disease (CAD). Compared to men, women appear to have greater susceptibility to chronic forms of psychosocial stress, extending beyond an increased incidence of mood disorders to include a 2- to 4-fold higher risk of stress-dependent myocardial infarction in women, and up to 10-fold higher risk of Takotsubo syndrome—a stress-dependent coronary-myocardial disorder most prevalent in post-menopausal women. Sex differences arise at all levels of the stress response: from initial perception of stress to behavioural, cognitive, and affective responses and longer-term disease outcomes. These fundamental differences involve interactions between chromosomal and gonadal determinants, (mal)adaptive epigenetic modulation across the lifespan (particularly in early life), and the extrinsic influences of socio-cultural, economic, and environmental factors. Pre-clinical investigations of biological mechanisms support distinct early life programming and a heightened corticolimbic-noradrenaline-neuroinflammatory reactivity in females vs. males, among implicated determinants of the chronic stress response. Unravelling the intrinsic molecular, cellular and systems biological basis of these differences, and their interactions with external lifestyle/socio-cultural determinants, can guide preventative and therapeutic strategies to better target coronary heart disease in a tailored sex-specific manner.

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The Effects of Stress and Diet on the “Brain–Gut” and “Gut–Brain” Pathways in Animal Models of Stress and Depression

Cited by 25 publications

References 150 publications

Gut microbiota and its metabolites in depression: from pathogenesis to treatment

Gut microbiota and its metabolites in depression: from pathogenesis to treatment

Blocking coprophagy increases the levels of inflammation and depression in healthy mice as well as mice receiving fecal microbiota transplantation from disease model mice donors

The sex-dependent response to psychosocial stress and ischaemic heart disease

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