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Maternal Weaning Modulates Emotional Behavior and Regulates the Gut-Brain Axis.
Evidence shows that nutritional and environmental stress stimuli during postnatal period influence brain development and interactions between gut and brain. In this study we show that in rats, prevention of weaning from maternal milk results in depressive-like behavior, which is accompanied by changes in the gut bacteria and host metabolism. Depressive-like behavior was studied using the forced-swim test on postnatal day (PND) 25 in rats either weaned on PND 21, or left with their mother until PND 25 (non-weaned). Non-weaned rats showed an increased immobility time consistent with a depressive phenotype. Fluorescence in situ hybridization showed non-weaned rats to harbor significantly lowered Clostridium histolyticum bacterial groups but exhibit marked stress-induced increases. Metabonomic analysis of urine from these animals revealed significant differences in the metabolic profiles, with biochemical phenotypes indicative of depression in the non-weaned animals. In addition, non-weaned rats showed resistance to stress-induced modulation of oxytocin receptors in amygdala nuclei, which is indicative of passive stress-coping mechanism. We conclude that delaying weaning results in alterations to the gut microbiota and global metabolic profiles which may contribute to a depressive phenotype and raise the issue that mood disorders at early developmental ages may reflect interplay between mammalian host and resident bacteria.
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Effects of arabinoxylan on BDNF/TrkB/p-CREB signaling pathway in the prefrontal cortex and intestinal microbiome in post-stroke depressed rats.
AIM: To explore the effects of arabinoxylan on the BDNF/TrkB/p-CREB signaling pathway in the prefrontal cortex of post-stroke depressed rats, and to explore its neuronal protective effects through the microbial-gut-brain axis in the regulation of this pathway. METHODS: The rat model of post-stroke depression (PSD) was established by middle cerebral artery occlusion (MCAO) combined with chronic unpredictable mild stimulation (CUMS). They were randomly divided into 5 groups (blank control, post-stroke depression, arabinoxylan, fluoxetine hydrochloride, fluoxetine hydrochloride combined arabinoxylan). The rats were treated differently for 28 days according to their grouping. Body mass, sugar and water consumption experiments and open-field experiments were used to evaluate the behavior of rats. The pathological changes were observed by H&E staining. The expression levels of amine neurotransmitters were detected by ELISA. The expression levels of BDNF mRNA and BDNF, TrkB and p-CREB were detected by RT-PCR and Western blot. The analysis of intestinal metagenomics was conducted by 16 S rDNA sequencing. RESULTS: Compared with the post-stroke depression group, the body weight, activity and sugar water consumption rate of the arabinoxylan group were increased. The expression levels of 5-HT in the prefrontal cortex, colon and serum levels of 5-HT, DA and NE were increased. The expression levels of BDNF mRNA and BDNF, TrkB and P-CREB in the prefrontal cortex were also upregulated. The number of neurons in the prefrontal cortex increased; Colon mucosal injury and inflammatory cell infiltration decreased, the intestinal microbial diversity increased; The relative abundance of probiotics such as bifidobacterium, Christensenia, Dubosiella New York and ruminococcus increased. The relative abundance of Prevotella NK3B31 group was reduced. The level of 5-HT in the prefrontal cortex was negatively correlated with the abundance of Prevotellaceae NK3B31 group. CONCLUSION: Arabinoxylan improved depressive-like behavior in rats and its neuroprotective role was achieved by promoting the growth of intestinal probiotics, improving the intestinal barrier, affecting the BDNF/TrkB/p-CREB signaling pathway, and increasing the expression levels of monoamine neurotransmitters 5-HT, DA and NE.
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Interplay Between Human Gut Bacteria Escherichia coli and Lactobacillus mucosae in the Occurrence of Neuropsychiatric Disorders in Mice.
To understand the roles of human gut bacteria in the occurrence of neuropsychiatric disorders, we isolated inflammatory Escherichia coli K1 and anti-inflammatory Lactobacillus mucosae from healthy human feces and examined their effects on the occurrence of altered microbiota, cognitive decline, and depression in mice. Oral gavage of Escherichia coli K1 caused colitis, cognitive decline, and depression in mice in the elevated plus maze, tail suspension, and forced swimming tasks. However, NK41 treatment reduced K1-induced cognitive decline and anxiety/depression. Furthermore, NK41 treatment increased K1-suppressed brain-derived neurotrophic factor (BDNF) expression and BDNF+/NeuN+ cell population and suppressed K1-induced NF-κB activation and LPS+/Iba1+ and NF-κB+/Iba1+ (microglial) cell populations in the hippocampus. NK41 treatment also suppressed K1-induced TNF-α and LPS levels in the blood and TNF-α expression, myeloperoxidase activity, NF-κB+/CD11c+ and CD11b+/CD11c+ cell populations in the colon. Furthermore, NK41 treatment decreased K1-induced colonic MUC2 expression, gut Proteobacteria population, and fecal LPS levels and modified the bacterial abundance related to polysaccharide breaking and biosynthesis. In conclusion, the overgrowth of inflammatory bacteria such as Escherichia coli in the gastrointestinal tract can cause neuropsychiatric disorders with gut microbiota alteration and the superiority of anti-inflammatory bacteria such as Lactobacillus mucosae can alleviate neuropsychiatric disorders with the attenuation of altered microbiota.
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Ovarian progesterone suppresses depression and anxiety-like behaviors by increasing the Lactobacillus population of gut microbiota in ovariectomized mice.
Depression and anxiety, which are severe symptoms during menopause, are caused by ceased ovarian activity and declined serum progesterone levels. Studies have demonstrated that gut microbiota can regulate brain function and change the microbiota composition during the perimenopause period. This study investigated whether progesterone affects depressant and anxious behaviors via gut microbiota. In ovariectomized (OVX) mice, treatment with progesterone improved depressive and anxious behaviors, and gut microbiota composition was significantly changed. In particular, increased Lactobacillus spp. were observed in these mice. Reduction of microbiota by antibiotic treatment abolished the effect of progesterone on depression and anxiety. In addition, administration of Lactobacillus (L.) reuteri that was increased by progesterone also reduced the depressant behavior in OVX mice, and BDNF gene expression was elevated by progesterone treatment and L. reuteri administration in the hippocampus. Moreover, we found that progesterone stimulated the growth of L. reuteri in vitro. In summary, our findings indicate that progesterone reduces depression and anxiety through changes in gut microbiota composition, particularly by increasing the Lactobacillus spp. population.
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Association between the Gut Microbiota and Depression in Asian Populations: A Systematic Review and Meta-Analysis.
INTRODUCTION: Depression is a major global health concern. Emerging evidence implicates the role of the gut-brain axis in the depression pathogenesis. However, the gut microbiota-depression association remains underinvestigated in Asian populations, where dietary habits, genetics, and environmental exposures differ from Western settings. This systematic review and meta-analysis assessed the association between gut microbiota and depression among Asians. METHODS: Five databases (PubMed, Embase, Scopus, Web of Science, and Cochrane) were searched through December 25, 2024. Observational studies comparing gut microbiota via sequencing in Asian individuals with depression versus healthy controls (HCs) were included. Data on α and β diversity and taxon-level differences were extracted. Standardized mean differences (SMDs) were computed for alpha diversity. Beta diversity and taxonomic findings were summarized narratively due to methodological heterogeneity. RESULTS: Of 2,557 records screened, 20 studies with 3,380 participants (1,298 depressed, 2,082 HCs) met inclusion criteria. Eighteen studies evaluated alpha diversity. A small but significant reduction in the Shannon index was detected among depressed individuals (SMD = -0.11; 95% CI: -0.19 to -0.02; p = 0.02), whereas other indices (Chao1, Simpson, ACE) revealed no significant differences. Among 16 studies examining beta diversity, 13 reported significant compositional differences. Phylum-level analysis consistently revealed increased Actinobacteria in depression, with variable trends in Firmicutes, Bacteroidetes, and Proteobacteria. Family-level trends included elevated Bifidobacteriaceae, Coriobacteriaceae, Enterobacteriaceae, and reduced Prevotellaceae, Rikenellaceae, and Veillonellaceae. CONCLUSIONS: Gut dysbiosis is associated with depression in Asian populations, reflecting reduced beneficial taxa and increased proinflammatory microbes, with implications for microbial biomarkers and therapeutic targets.
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Berberine Alleviates Chronic Restraint Stress-Induced Depression-Like Behavior by Modulating Gut Microbiota and SCFA Production in Mice.
The exact mechanism by which berberine alleviates depression remains unclear. In this study, we explored the relationship between the antidepressant effect of berberine and the microbiota-brain-gut axis. The levels of IL-1β, TNF-α, IL-6, corticosterone, serotonin, and brain-derived neurotrophic factor (BDNF) were quantified using enzyme-linked immunosorbent assays (ELISA) and Western blotting. Variations in the composition of the gut microbiota were examined using 16S rRNA gene sequencing. Berberine significantly mitigated depressive behaviors in mice with CRS, as manifested by increased total distance traveled and central zone duration in the open-field examination, increased time and number of entries into the outstretched arms during the elevated and maze tests, and an increase in the exercise time during the tail suspension and forced swimming tests. Histopathological analysis indicated that berberine ameliorated CRS-induced hippocampal and colonic damage in mice. Additionally, berberine substantially restrained the generation of proinflammatory cytokines and corticosterone in mice with CRS, while increasing the levels of BDNF and serotonin. Importantly, berberine significantly ameliorated CRS-induced depression-like behaviors (p < 0.01) and restored gut microbial diversity and short-chain fatty acid (SCFA) levels (fold-change: acetate 1.8-fold, butyrate 2.2-fold; p < 0.05). Furthermore, berberine restored the CRS-induced alterations in SCFA production. Our results indicate that berberine may exert antidepressant effects via a pleiotropic mechanism that modulates the microbiome-brain-gut axis.
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Increased efficacy of combining prebiotic and postbiotic in mouse models relevant to autism and depression.
The Microbiota-Gut-Brain axis (MGBA) is a bidirectional communication pathway between gut bacteria and the central nervous system (CNS) (including the intestine) that exerts a profound influence on neural development, neuroinflammation, activation of stress response and neurotransmission, in addition to modulating complex behaviours, such as sociability and anxiety. Several MGBA modulating approaches are possible, such as probiotic administration. A reasonable pharmacological approach would also be the contemporarily administration of both prebiotics and postbiotics. To test this hypothesis, we probed the effects of α-lactalbumin (ALAC; a prebiotic in the dose range of 125-500 mg/kg) and sodium butyrate (NaB; a postbiotic in the dose range of 30-300 mg/kg) alone and in combination. We used two animal behavioural models of idiopathic autism, (BTBR mice) and anxiety/depression (chronic unexpected mild stress - CUMS mice) respectively, using several standard behavioural paradigms such as Three-chamber social interaction test, Marble burying assay, depression-, anxiety- and memory-tests. In BTBR autistic mice, we found that both ALAC and NaB improve animal sociability, and memory in the passive avoidance (PA); drug combination was more effective in almost all tests also reducing immobility time in the forced swimming test (FST), which was not affected by single drug administration. Similarly, in the CUMS mice, single drug administration was effective in improving: 1) depressive-like behaviour in the FST and sucrose preference test; 2) memory and learning in the PA, novel object recognition and Morris water maze tests. Drug combination was again more effective than single drug administration in most cases; however, in the CUMS model, neither single drug or combination was effective in the elevated plus maze test for anxiety. Our results suggest that in both models, ALAC and NaB combination is more effective in improving some pathological aspects of animal behaviour than single administration and that the prebiotic/postbiotic approach should be considered a reasonable approach for the manipulation of the MGBA to improve efficacy.
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Gut microbiota modulates depressive-like behaviors induced by chronic ethanol exposure through short-chain fatty acids.
BACKGROUND: Chronic ethanol exposure (CEE) is recognized as an important risk factor for depression, and the gut-brain axis has emerged as a key mechanism underlying chronic ethanol exposure-induced anxiety and depression-like behaviors. Short-chain fatty acids (SCFAs), which are the key metabolites generated by gut microbiota from insoluble dietary fiber, exert protective roles on the central nervous system, including the reduction of neuroinflammation. However, the link between gut microbial disturbances caused by chronic ethanol exposure, production of SCFAs, and anxiety and depression-like behaviors remains unclear. METHODS: Initially, a 90-day chronic ethanol exposure model was established, followed by fecal microbiota transplantation model, which was supplemented with SCFAs via gavage. Anxiety and depression-like behaviors were determined by open field test, forced swim test, and elevated plus-maze. Serum and intestinal SCFAs levels were quantified using GC-MS. Changes in related indicators, including the intestinal barrier, intestinal inflammation, neuroinflammation, neurotrophy, and nerve damage, were detected using Western blotting, immunofluorescence, and Nissl staining. RESULTS: Chronic ethanol exposure disrupted with gut microbial homeostasis, reduced the production of SCFAs, and led to anxiety and depression-like behaviors. Recipient mice transplanted with fecal microbiota that had been affected by chronic ethanol exposure exhibited impaired intestinal structure and function, low levels of SCFAs, intestinal inflammation, activation of neuroinflammation, a compromised blood-brain barrier, neurotrophic defects, alterations in the GABA system, anxiety and depression-like behaviors. Notably, the negative effects observed in these recipient mice were significantly alleviated through the supplementation of SCFAs. CONCLUSION: SCFAs not only mitigate damage to intestinal structure and function but also alleviate various lesions in the central nervous system, such as neuroinflammation, and reduce anxiety and depression-like behaviors, which were triggered by transplantation with fecal microbiota that had been affected by chronic ethanol exposure, adding more support that SCFAs serve as a bridge between the gut and the brain.
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Gut bacteria linked to mental well-being and depression.
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The Putative Antidepressant Mechanisms of Probiotic Bacteria: Relevant Genes and Proteins.
Probiotic bacteria are widely accepted as therapeutic agents against inflammatory bowel diseases for their immunostimulating effects. In the last decade, more evidence has emerged supporting the positive effects of probiotics on the course of neurodegenerative and psychiatric diseases. This brief review summarizes the data from clinical studies of probiotics possessing antidepressant properties and focuses on the potential genes and proteins underlying these mechanisms. Data from small-sample placebo-controlled pilot studies indicate that certain strains of bacteria can significantly reduce the symptoms of depression, especially in depressed patients. Despite the disparity between studies attempting to pinpoint the bacterial putative genes and proteins accounting for these mechanisms, they ultimately show that bacteria are a potential source of metabiotics-microbial metabolites or structural components. Since the constituents of cells-namely, secreted proteins, peptides and cell wall components-are most likely to be entangled in the gut-brain axis, they can serve as starting point in the search for probiotics with concrete properties.