Microbiota alteration is associated with the development of stress-induced despair behavior
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA644675 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12170400_1.fastq.gz | Fastqsanger.gz | |||
| SRR12170400_2.fastq.gz | Fastqsanger.gz | |||
| SRR12170401_1.fastq.gz | Fastqsanger.gz | |||
| SRR12170401_2.fastq.gz | Fastqsanger.gz | |||
| SRR12170402_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 208 |
Similar Datasets
Project description:Depressive disorders often run in families, which, in addition to the genetic component, may point to the microbiome as a causative agent. Here, we employed a combination of behavioral, molecular and computational techniques to test the role of the microbiota in mediating despair behavior. In chronically stressed mice displaying despair behavior, we found that the microbiota composition and the metabolic signature dramatically change. Specifically, we observed reduced Lactobacillus and increased circulating kynurenine levels as the most prominent changes in stressed mice. Restoring intestinal Lactobacillus levels was sufficient to improve the metabolic alterations and behavioral abnormalities. Mechanistically, we identified that Lactobacillus-derived reactive oxygen species may suppress host kynurenine metabolism, by inhibiting the expression of the metabolizing enzyme, IDO1, in the intestine. Moreover, maintaining elevated kynurenine levels during Lactobacillus supplementation diminished the treatment benefits. Collectively, our data provide a mechanistic scenario for how a microbiota player (Lactobacillus) may contribute to regulating metabolism and resilience during stress.
2020-07-08 | GSE153992 | GEO
Project description:Depressive disorders often run in families, which, in addition to the genetic component, may point to the microbiome as a causative agent. Here, we employed a combination of behavioral, molecular and computational techniques to test the role of the microbiota in mediating despair behavior. In chronically stressed mice displaying despair behavior, we found that the microbiota composition and the metabolic signature dramatically change. Specifically, we observed reduced Lactobacillus and increased circulating kynurenine levels as the most prominent changes in stressed mice. Restoring intestinal Lactobacillus levels was sufficient to improve the metabolic alterations and behavioral abnormalities. Mechanistically, we identified that Lactobacillus-derived reactive oxygen species may suppress host kynurenine metabolism, by inhibiting the expression of the metabolizing enzyme, IDO1, in the intestine. Moreover, maintaining elevated kynurenine levels during Lactobacillus supplementation diminished the treatment benefits. Collectively, our data provide a mechanistic scenario for how a microbiota player (Lactobacillus) may contribute to regulating metabolism and resilience during stress.
| S-EPMC5339726 | biostudies-literature
Project description:Differential behavior responses and genetic alteration underpinning exercise effectiveness in stress-susceptible mice
| PRJNA1192959 | ENA
Project description:Stress susceptibility varies across individuals, influenced by genetic, molecular, and environmental factors. Considering the individual differences in response to stress, however, approaches for exercise treatment as an antidepressant and anxiolytic intervention are also not exempt from variability in effectiveness among individuals, and insight into the biology of those variations can be gained by examining the individual adaptation to exercise. Here, we investigated the efficacy of voluntary wheel running (VWR) exercise as a disease-modifying intervention for stress-susceptible (SS) mice subjected to chronic restraint stress (CRST). Multidimensional behavior analysis revealed significant variability in the efficacy of VWR among individuals, with some mice showing substantial behavior phenotypic improvements (e.g., behavior despair, anhedonia, aversion to open space, and compulsive behavior) (SES) while others displayed limited or no benefits (SER). Furthermore, transcriptomic analysis of the ventral hippocampus (vHPC), a critical brain region involved in emotional regulation and processing, demonstrated that SES mice exhibited molecular signatures promoting adaptive changes by restoring cellular repair, energy availability, and synaptic plasticity observed in SS mice, whereas SER mice exhibited limited behavior resilience and distinct transcriptomic profiles enriched in structural adaptation without functional resilience and glia cell differentiation, particularly marked by astrocyte activation or differentiation. These findings suggest that while VWR can alleviate multiple concurrent behavior symptoms in stress-susceptible mice; however, its efficacy is influenced by distinct biological processes. Collectively, our work highlights the importance of a multivariate framework for behavior assessment and genetic underpinnings to better understand the often-overlooked variability in response to stress and the therapeutic efficacy of exercise in stress-related disorders.
2024-12-04 | GSE283250 | GEO
Project description:Chronic stress induces adaptive changes in the brain via the cumulative action of glucocorticoids, which is associated with mood disorders. Here we show that repeated daily five-minute restraint resolves pre-existing stress-induced depressive-like behavior in mice. Repeated injection of glucocorticoids in low doses mimics the anti-depressive effects of short-term stress. Repeated exposure to short-term stress and injection of glucocorticoids activate neurons in largely overlapping regions of the brain, as shown by c-Fos staining, and reverse distinct stress-induced gene expression profiles. Chemogenetic inhibition of neurons in the prelimbic cortex projecting to the nucleus accumbens, basolateral amygdala, or bed nucleus of the stria terminalis results in anti-depressive effects similarly to short-term stress exposure, while only inhibition of neurons in the prelimbic cortex projecting to the bed nucleus of the stria terminalis rescues glucocorticoid release. In summary, we show that short-term stress can reverse adaptively altered stress gains and resolve stress-induced depressive-like behavior.
2021-09-09 | GSE183624 | GEO
Project description:Intergenerational stress increases lifetime susceptibility to depression and other psychiatric disorders. Whether intergenerational stress transmission is a consequence of in-utero neurodevelopmental disruptions or early-life mother-infant interaction is largely unknown, due to the complexity, superposition, and inseparability between the prenatal and postnatal mechanisms. Here we show that prenatal stress, through exposing pregnant mice to predator scent, induces depressive-like behavior and social deficits. Cross-fostering experiments indicate divergent and convergent mechanisms of both in utero and early-life parenting environments and support a two-hit model of stress transmission. According to this model, prenatal stress (first-hit) primes brain metabolome and transcriptome (metabotranscriptome), and increases vulnerability to the second-hit in early life, triggered by poor caregiving by the traumatized mothers. Metabolomics, transcriptomic and bioinformatics analyses reveal mechanisms that involve stress- and hypoxia- response metabolic pathways in the brains of the newborn mice, likely through the production of the epigenetic modifiers 2-Hydroxyglutaric acid and succinic acid. These responses produce long-lasting alterations in mitochondrial-energy metabolism, and epigenetic processes pertaining to DNA and chromatin modifications. We demonstrate that an early pharmacological intervention – correction of the mitochondria metabolism, and epigenetic modifications with acetyl-L-carnitine (ALCAR) supplementation - produces long-lasting protection against the behavioral deficits associated with intergenerational transmission of traumatic stress.
2021-04-01 | GSE171275 | GEO
Project description:Microbiota alteration upon blueberry consumption
| PRJNA679320 | ENA
Project description:Dynamic behavior of the epigenetic machinery upon thermal stress
| PRJNA496026 | ENA
Project description:Acute stress-induced anxiety is an important way for animals to avoid danger. However, neural and molecular mechanisms that underlie control of anxiety behavior are largely elusive. Here, we find acute physical stress activates a large number of neurons in the primary somatosensory cortex, trunk region (S1Tr). Single-cell sequencing reveals the S1Tr c-fos positive neurons activated by acute stress are largely GABAergic somatostatin (Sst) neurons. These S1TrSst neurons activated by acute stress showed desensitization during subsequent anxiety-like behavior tests. Selective inhibition or apoptosis of S1TrSst neurons mimics acute stress effects to induce anxiety. In contrast, selective activation of S1TrSst neurons reduced acute stress-induced anxiety. Furthermore, we demonstrate that S1TrSst cells receive inputs from the secondary auditory cortex, dorsal area (AUD) GABAergic neurons to modulate acute stress-induced anxiety. Finally, from the results of spatial transcriptome sequencing and precise projection-specificity Pde4b protein knockdown strategy, we show that acute stress reduces Pde4b-regulated cyclic adenosine monophosphate (cAMP) signaling pathway activity in the AUDGABA-S1TrSst projections and resulting in a hypoactivity of S1TrSst neurons during subsequent behavioral tests. Our study unveils a neural and molecular mechanism for acute stress-elicited anxiety and affords a theoretical basis for clinical treatment of anxiety disorders.
2025-01-03 | GSE285650 | GEO
Project description:Acute stress-induced anxiety is an important way for animals to avoid danger. However, neural and molecular mechanisms that underlie control of anxiety behavior are largely elusive. Here, we find acute physical stress activates a large number of neurons in the primary somatosensory cortex, trunk region (S1Tr). Single-cell sequencing reveals the S1Tr c-fos positive neurons activated by acute stress are largely GABAergic somatostatin (Sst) neurons. These S1TrSst neurons activated by acute stress showed desensitization during subsequent anxiety-like behavior tests. Selective inhibition or apoptosis of S1TrSst neurons mimics acute stress effects to induce anxiety. In contrast, selective activation of S1TrSst neurons reduced acute stress-induced anxiety. Furthermore, we demonstrate that S1TrSst cells receive inputs from the secondary auditory cortex, dorsal area (AUD) GABAergic neurons to modulate acute stress-induced anxiety. Finally, from the results of spatial transcriptome sequencing and precise projection-specificity Pde4b protein knockdown strategy, we show that acute stress reduces Pde4b-regulated cyclic adenosine monophosphate (cAMP) signaling pathway activity in the AUDGABA-S1TrSst projections and resulting in a hypoactivity of S1TrSst neurons during subsequent behavioral tests. Our study unveils a neural and molecular mechanism for acute stress-elicited anxiety and affords a theoretical basis for clinical treatment of anxiety disorders.
2025-01-02 | GSE285495 | GEO