Project description:In order to better understand the effects of social stress on the prefrontal cortex, we investigated gene expression in mice subjected to acute and repeated social encounters of different duration using microarrays. The observed up-regulation of genes associated with vascular system and brain injury suggests that stressful social encounters may affect brain function through the stress-induced dysfunction of the vascular system. We studied gene expression profiles of prefrontal cortices of male mice subjected to social stress of different durations: Comparisons included: acute stress (24 hours after single social stress episode) vs. acute control (unstressed), stress-8 days vs. control-8 days, stress-13 days vs. control-13 days, stress-13 days+5 days of rest vs. control-13 days+5 days of rest. For each comparison, we analyzed 3 biological replicates per group. Two of out of three biological replicates were further replicated in dye swap (final dye swap failed due to problem during microarray hybridization). Each biological replicate consisted of equal amounts of total RNA from 3 mice subjected to the same experimental condition.
Project description:Chronic stress increases the risk of emotional disorders by altering brain structure and function. Patients with post-traumatic stress disorder (PTSD) or depressions show activity difference between the two hemispheres in the prefrontal cortex (PFC) but molecular targets associated with this laterality remains unclear. Here, we reveal that chronic social defeats later gene-expression profile differentially between the left and right medial prefrontal cortices (mPFC) in mice.
Project description:In order to better understand the effects of social stress on the prefrontal cortex, we investigated gene expression in mice subjected to acute and repeated social encounters of different duration using microarrays. The observed up-regulation of genes associated with vascular system and brain injury suggests that stressful social encounters may affect brain function through the stress-induced dysfunction of the vascular system. The study was supported by Grant N N311 604938, 2011/03/N/NZ29/05222 and partially by IP2011 030371. Statistical analysis of microarray data was supported with Grant N N519 657940.
Project description:To examine ketamine’s long-lasting effects on gene expression in the brains of mice exhibiting depression-like behaviors, we used spatial transcriptomics (ST) to analyze transcriptomics on the cortices of mice exposed to chronic social defeat stress (CSDS) and treated with ketamine.
Project description:This study explored the interaction of early life and adult stress on transcriptional and chromosomal states in a 2x2 design. Male and female mice were subjected to early life stress (ELS) or were standard-reared (Std), were housed normally through adolescence, and were then exposed to 10 days of control (Ctl) or chronic social defeat stress (CSDS: males only) or 3 days of sub-threshold variable stress (STVS: females only) conditions in adulthood. Long-lasting transcriptional alterations were assessed in the ventral tegmental area (VTA), nucleus accumbens (NAc), medial prefrontal cortex (PFC), and ventral hippocampus (HIP, males only) in adulthood.
Project description:Major depressive disorder is a common mood disorder. Chronic stressful life is presumably main etiology that leads to the neuron and synapse atrophies in the limbic system. However, the intermediate molecules from stress to neural atrophy remain elusive. Mice were treated by chronic unpredictable mild stress (CUMS) until demonstrating depression-like behaviors confirmed by the tests of sucrose preference, forced swimming and Y-maze. The sequencings of microRNA and mRNA from the medial prefrontal cortices were performed in CUMS-induced depression mice versus control mice to assess the molecular profiles of major depressive disorder. In the medial prefrontal cortices of depression-like mice, the levels of mRNAs that translated the proteins for the GABAergic synapses, dopaminergic synapses, myelination, synaptic vesicle cycle and neuronal growth were downregulated. miRNAs of regulating these mRNAs are upregulated. The deterioration of GABAergic and dopaminergic synapses as well as axonal growth is associated to CUMS-induced depression.
Project description:Major depressive disorder is a common mood disorder. Chronic stressful life is presumably main etiology that leads to the neuron and synapse atrophies in the limbic system. However, the intermediate molecules from stress to neural atrophy remain elusive. Mice were treated by chronic unpredictable mild stress (CUMS) until demonstrating depression-like behaviors confirmed by the tests of sucrose preference, forced swimming and Y-maze. The sequencings of microRNA and mRNA from the medial prefrontal cortices were performed in CUMS-induced depression mice versus control mice to assess the molecular profiles of major depressive disorder. In the medial prefrontal cortices of depression-like mice, the levels of mRNAs that translated the proteins for the GABAergic synapses, dopaminergic synapses, myelination, synaptic vesicle cycle and neuronal growth were downregulated. miRNAs of regulating these mRNAs are upregulated. The deterioration of GABAergic and dopaminergic synapses as well as axonal growth is associated to CUMS-induced depression.
Project description:We performed high-throughput profiling of gene expression in the anterior cingulate cortex of stress-vulnerable BALB/c mice subjected to social defeat stress. BALB/c mice were subjected to 5-day of social defeat stress and euthanized for tissue collection. We then conducted the transcriptomics analysis. Our study provided insights into the understanding of the molecular mechanisms underlying the behavioral response to stress.
