Mus musculus
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ABSTRACT:
PROVIDER: PRJNA390653 | ENA |
REPOSITORIES: ENA
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Project description:Ppm1f is regulated by stress and associated with anxiety and depression [amygdala]
| PRJNA390652 | ENA
Project description:Ppm1f is regulated by stress and associated with anxiety and depression
| PRJNA390645 | ENA
Project description:Despite studies providing insight into the neurobiology of chronic stress, depression and anxiety, long noncoding RNA (lncRNA)-mediated mechanisms underlying the common and distinct pathophysiology of these stress-induced disorders remain nonconclusive. In a previous study, we used the chronic mild stress paradigm to separate depression-susceptible, anxiety-susceptible and insusceptible rat subpopulations. In the current study, lncRNA and messenger RNA (mRNA) expression was comparatively profiled in the hippocampus of the three stress groups using microarray technology. Groupwise comparisons identified distinct sets of lncRNAs and mRNAs associated with the three different behavioral phenotypes of the stressed rats. To investigate the regulatory roles of the dysregulated lncRNAs upon mRNA expression, correlations between the differential lncRNAs and mRNAs were first analyzed by combined use of weighted gene coexpression network analysis and ceRNA theory-based methods. Subsequent functional analysis of strongly correlated mRNAs indicated that the dysregulated lncRNAs were involved in various biological pathways and processes to specifically induce rat susceptibility or resiliency to depression or anxiety. Further intersectional analysis of phenotype-associated and drug-associated lncRNA-mRNA networks and subnetworks assisted in identifying 16 hub lncRNAs as potential targets of anti-depression/anxiety drugs. Collectively, our study established the molecular basis for understanding the similarities and differences in pathophysiological mechanisms underlying stress-induced depression or anxiety and stress resiliency, revealing several important lncRNAs that represent potentially new therapeutic drug targets for depression and anxiety disorders.
2020-08-21 | GSE156580 | GEO
Project description:Neuropathic pain is a complex chronic condition, characterized by a wide range of sensory, cognitive, and affective symptoms. Indeed, a large percentage of neuropathic pain patients are also afflicted with depression and anxiety disorders -- a pattern that is reliably replicated in animal models. Mounting evidence from clinical and preclinical studies indicates that chronic pain corresponds with adaptations in several brain networks involved in mood, motivation, and reward. Chronic stress is also a major determinant for depression. However, whether chronic pain and chronic stress affect similar mechanisms, and whether chronic pain can affect gene expression patterns known to be involved in depression, remains poorly understood. We employed the spared nerve injury model (SNI) of neuropathic pain in adult C57BL\6 mice and performed next-generation RNA-sequencing in order to monitor changes in gene expression in three brain regions known to be implicated in the pathophysiology of depression and in the modulation of pain: the nucleus accumbens (NAc), the medial prefrontal cortex (mPFC), and the periaqueductal grey (PAG). We observed mostly unique transcriptome profiles across the three brain regions but found common intracellular signal transduction pathways and biological functions were affected. A large amount of genes showing SNI-induced altered expression have been implicated in depression, anxiety, or chronic pain. In addition, we identified genes that are similarly regulated in a murine model of depression: chronic unpredictable stress. Our study provides the first unbiased characterization of neuropathic pain-induced long-term gene expression changes in three distinct brain regions, and presents evidence that neuropathic pain affects the expression of several genes that are also regulated by chronic stress.
2017-09-06 | GSE91396 | GEO
Project description:Gene expression profiling of blood cells in patients with major depressive disorder (MDD) has been used to identify potential biomarkers and to address the pathophysiology of MDD. However, whether alteration in gene expression in blood cells are reflected in the brain of the same individual is unclear. Here, we used an animal model of depression to investigate intra-subject correlation of gene expression patterns between the whole blood (WB) and the medial prefrontal cortex (mPFC). Ovariectomized mice exposed to the chronic ultra-mild stress were used as an animal model of depression. The major findings of the current genome-wide microarray analysis are that 1) the expression levels of 467 genes that were expressed in both tissues correlated positively between the two tissues, 2) alterations in the expression of 4,215 genes in the WB of OVX-operated mice compared to the sham-operated mice were concordant with alterations in the corresponding mPFC, 3) the biological terms over-represented in the 4,215 OVX-affected genes were associated with ribosomal function, and 4) the 6 genes that are potentially relevant to depression-like behavior were observed to be differentially expressed in the WB of the model mice. The current findings suggest that alterations in the expression of a subset of genes are significantly correlated between the WB and the mPFC with in the same individual in an experimental model of depression. Female mice were subjected to chronic ultra-mild stress, a bilateral ovariectomy, or both. Sham-operated mice without stress were used as the control. Medial prefrontal cortex and whole blood were obtained from the same individual (n = 6 in each group), and analyzed using an Agilent SurePrint G3 Mouse GE 8×60K Microarray (Design ID: 028005)
2015-08-21 | E-GEOD-72262 | biostudies-arrayexpress
Project description:Rnf41 is associated with anxiety like behavior, major depression and beta carboline induced seizure
| PRJNA101827 | ENA
Project description:Stress is associated with an increased prevalence of anxiety and depression. Repeated social defeat (RSD) stress in mice increases the release of monocytes from the bone marrow that are recruited to the brain by microglia. These monocytes enhance inflammatory signaling and augment anxiety. Moreover, RSD promotes stress sensitization, in which exposure to acute stress 24 days after cessation of RSD causes anxiety recurrence. The purpose of this study was to determine whether microglia were critical to stress sensitization and exhibited altered gene expression 24 days after RSD.
2018-12-21 | GSE124169 | GEO
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Hormonal fluctuations throughout the ovarian cycle contribute to femalesâ?? higher vulnerability to anxiety disorders when compared to males. Notably, such sex differences are controlled by regulation of genes in the medial prefrontal cortex (mPFC) including the transcription factor early growth response 1 (Egr1) in rats, which highlights a control of anxiety-like behaviors by sexually-biased gene expression. We therefore undertook a large-scale characterization of sex differences and their interaction with the estrous cycle in the adult mPFC transcriptome and report that proestrus and diestrus females (with high and low ovarian hormones levels, respectively) exhibited a partly-opposed sexually-biased transcriptome. Surprisingly, the extent of regulations within females vastly exceeded sex differences, and support a multi-level reorganization of synaptic function across the estrous cycle. Furthermore, genome-wide analysis of Egr1 binding highlighted its role in controlling the synapse-related genes varying within females, and the sex- and estrous cycle-dependent transcriptomic reorganization in the rat mPFC. Early growth response 1 (Egr1) binding profiling in the adult rat medial prefrontal cortex of males, proestrus females, and diestrus females. A total of 9 animals were used, corresponding to 3 Males, 2 proestrus females, and 4 diestrus females.
2015-10-23 | E-GEOD-69772 | biostudies-arrayexpress
Project description:Stressful circumstances are significant contributors to mental illnesses, such as major depressive disorder. Anhedonia, which is the loss of the ability to enjoy pleasure, including rewarding activities or social contexts, is considered a key symptom of depression. Although stress-induced depression is associated with anhedonia in humans and animals, the underlying molecular mechanisms of anhedonic responses remain poorly understood. In this study, we conducted RNA sequencing to profile the medial prefrontal cortex which was substantially associated with the CUS-induced anhedonic behavioral phenotypes. Employing chronic unpredictable stress (CUS), we determined two subpopulations based on sucrose preference, which was highly correlated with social reward: susceptible (SUS, anhedonic) vs. resilient (RES, non-anhedonic) groups. We identified Syt4 as a hub gene in a gene network unique to anhedonia by conducting a weighted gene co-expression network analysis of the RNA sequencing data from the mPFC of SUS and RES mice. We also confirmed that Syt4 overexpression in the mPFC was pro-susceptible, while the Syt4 knockdown was pro-resilient; the pro-susceptible effects of SYT4 were mediated through the reduction of brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase B (TrkB) signaling in the mPFC. These findings suggested that SYT4-BDNF interactions in the mPFC could be a crucial regulatory mechanism of anhedonic susceptibility to chronic stress.
2024-03-06 | GSE226576 | GEO