scholarly journals Effects of Chronic Social Defeat Stress on Behavior and Dopamine Receptors in Adolescent Mice With 6-Hydroxydopamine Lesions of the Medial Prefrontal Cortex

2021 ◽  
Vol 15 ◽  
Author(s):  
Tong Zhao ◽  
XiaoLei Gao ◽  
Guang-Biao Huang
Keyword(s):  
Cognitive Impairment ◽  
Dopamine Receptors ◽  
Social Stress ◽  
Social Cognitive ◽  
Social Defeat ◽  
Stress Factors ◽  
Control Group ◽  
Social Defeat Stress ◽  
Chronic Social Defeat Stress ◽  
6 Hydroxydopamine

Background: Social stress factors in schizophrenia have long-term effects, but will only induce symptoms in a portion of individuals, even if exposed to identical stress.Methods: In the current experiment, we examined mice with 6-hydroxydopamine (6-OHDA)-induced medial prefrontal cortical (mPFC) injury to select for members of a “stress-susceptible group,” and observed the changes in their behavior and the expression of D1 and D2 dopamine receptors in the amygdala and hippocampus.Results: We observed that after chronic social defeat stress, 72.6% of the 6-OHDA lesioned mice exhibited stress response to aggressors, compared to 52.3% of the blank control group. Both the 6-OHDA lesion + social defeat and social defeat groups exhibited anxiety and depression-like behavior. However, social cognitive impairment in the mice from the 6-OHDA lesion + social defeat group was more significant and the D1 expression levels in the amygdala were significantly decreased.Conclusion: These results suggest that the reason that adolescent mice with cortical injury were highly sensitive to defeat stress and had more prominent social cognitive impairment may be the decreased selectivity of D1 in the amygdala.

scholarly journals Dysfunction in Ribosomal Gene Expression in the Hypothalamus and Hippocampus following Chronic Social Defeat Stress in Male Mice as Revealed by RNA-Seq

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Dmitry A. Smagin ◽  
Irina L. Kovalenko ◽  
Anna G. Galyamina ◽  
Anatoly O. Bragin ◽  
Yuriy L. Orlov ◽  
...  
Keyword(s):  
Gene Expression ◽  
Social Stress ◽  
Ribosome Biogenesis ◽  
Social Defeat ◽  
Brain Regions ◽  
Ribosomal Gene ◽  
Rna Seq ◽  
Male Mice ◽  
Social Defeat Stress ◽  
Chronic Social Defeat Stress

Chronic social defeat stress leads to the development of anxiety- and depression-like states in male mice and is accompanied by numerous molecular changes in brain. The influence of 21-day period of social stress on ribosomal gene expression in five brain regions was studied using the RNA-Seq database. MostRps, Rpl, Mprs, andMprlgenes were upregulated in the hypothalamus and downregulated in the hippocampus, which may indicate ribosomal dysfunction following chronic social defeat stress. There were no differentially expressed ribosomal genes in the ventral tegmental area, midbrain raphe nuclei, or striatum. This approach may be used to identify a pharmacological treatment of ribosome biogenesis abnormalities in the brain of patients with “ribosomopathies.”

scholarly journals Upregulation of miR-195a inhibits brain-derived neurotrophic factor in mouse hippocampus and may contribute to depression-like behaviors induced by chronic social stress

2021 ◽  
Vol 19 (12) ◽  
pp. 2537-2543
Author(s):  
Xuping Wen ◽  
Mingshuan Lin
Keyword(s):  
Protein Expression ◽  
Neurotrophic Factor ◽  
Social Defeat ◽  
Brain Derived Neurotrophic Factor ◽  
Luciferase Reporter ◽  
Control Group ◽  
Social Defeat Stress ◽  
Chronic Social Defeat Stress ◽  
Mouse Hippocampus

Purpose: To explore the effect of miR-195a on nerve cells in the hippocampal region of depressionmodel mice.Methods: A chronic social defeat stress (CSDS) model was used as a depressed mouse model. In vivo, C57BL/6J mice received CSDS treatment or miR-195a antagomir. Depression-like behaviors were evaluated. In vitro, the target relationship between miR-195a and brain-derived neurotrophic factor (BDNF) was validated by luciferase reporter assays in HEK-293 cells. In primary cortical neurons, expression levels of miR-195a and BDNF mRNA were evaluated using quantitative polymerase chain reaction (qPCR). BDNF protein expression was determined by western blotting.Results: The sucrose preference ratio and social contact of the CSDS group were significantly decreased, whereas the immobility time was significantly increased, compared with the control group (p< 0.05). Interestingly, the expression of miR-195a was upregulated in the CSDS group compared with control group (p < 0.05). Bioinformatics prediction and luciferase reporter assay data indicate that miR195a bound the BDNF 3’ untranslated region. BDNF protein expression levels were significantly reduced by miR-195a mimic but increased by miR-195a inhibitor, compared with the negative control mimic group (p < 0.05). In vivo, miR-195a antagomir alleviated depression-like behaviors compared with CSDS group. In addition, miR-195a antagomir restored the expression of BDNF in mouse hippocampus in the CSDS group (p < 0.05).Conclusion: MiR-195a inhibitor ameliorates depression-like behaviors of depressed mice by downregulation of BDNF, whereas  upregulation of miR-195a inhibits BDNF expression in mouse hippocampus and may contribute to depression. Keywords: Chronic social defeat stress, Depression, MiR-195, brain-derived neurotrophic factor, BDNF 

scholarly journals Effects of chronic social defeat stress on behaviour, endoplasmic reticulum proteins and choline acetyltransferase in adolescent mice

2013 ◽  
Vol 16 (7) ◽  
pp. 1635-1647 ◽  
Author(s):  
Guang-Biao Huang ◽  
Tong Zhao ◽  
Sushma Shrestha Muna ◽  
Tarique Rajasaheb Bagalkot ◽  
Hong-Mei Jin ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Western Blotting ◽  
Choline Acetyltransferase ◽  
Stress Proteins ◽  
Social Defeat ◽  
Adolescent Male ◽  
Control Group ◽  
Social Defeat Stress ◽  
Chronic Social Defeat Stress ◽  
Behavioural Tests

Abstract The present study investigated the effects of social defeat stress on the behaviours and expressions of 78-kDa glucose-regulated protein (Grp78), CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) and choline acetyltransferase (Chat) in the brains of adolescent mice. Adolescent male C57BL/6J mice were divided into two groups (susceptible and unsusceptible) after 10 d social defeat stress. In expt 1, behavioural tests were conducted and brains were processed for Western blotting on day 21 after stress. In expt 2, social avoidance tests were conducted and brains were subsequently processed for Western blotting on day 12 after stress. Chronic social defeat stress produced more pronounced depression-like behaviours such as decreased locomotion and social interaction, increased anxiety-like behaviours and immobility, and impaired memory performance in susceptible mice. Moreover, susceptible mice showed greater expression of Grp78 and CHOP in the amygdala (Amyg) on days 12 and 21 compared with the other groups. Susceptible and unsusceptible groups showed significant increases in Grp78 and CHOP expression in the prefrontal cortex (PFC) and hippocampus (Hipp) on day 12 compared with the control group; this persisted until day 21. The levels of Chat measured on days 12 and 21 were significantly lower in the PFC, Amyg and Hipp of all defeated mice compared with controls. The findings of the behavioural tests indicate that chronic social defeat in adolescents produces anxiety-like behaviours, social withdrawal, despair-like behaviours and cognitive impairment. The Grp78, CHOP and Chat results suggest that the selective response of endoplasmic reticulum stress proteins in the Amyg plays an important role in the vulnerability–stress model of depression.

scholarly journals What it takes to be at the top: The interrelationship between chronic social stress and social dominance

2020 ◽  
Author(s):  
Merima Šabanović ◽  
He Liu ◽  
Vongai Mlambo ◽  
Hala Aqel ◽  
Dipesh Chaudhury
Keyword(s):  
Social Interaction ◽  
Social Stress ◽  
Social Preference ◽  
Social Rank ◽  
Social Defeat ◽  
Social Defeat Stress ◽  
Chronic Social Stress ◽  
Hierarchy Formation ◽  
Chronic Social Defeat Stress ◽  
Stress Susceptibility

AbstractDominance hierarchies of social animal groups are influenced by complex factors such as stress. Stress experienced by an animal prior to social interactions with a conspecific may be a determinant of their future social dynamics. Additionally, long-term occupancy of a specific hierarchical rank can have psychophysiological effects, leading to vulnerability to future stress.The current study aimed to delineate differential effects of stress acting before or after hierarchy formation. Using the chronic social defeat stress (CSDS) paradigm we performed behavioural investigations to determine whether exposure to CSDS before hierarchy formation predicted the new dominance status. Moreover, in another study we investigated whether social rank predicted stress vulnerability.We found that CSDS did not impede the establishment of dominance in new hierarchies as both stress-susceptible (socially avoidant) and –resilient (social) mice were able to attain dominant ranks. In contrast, within newly established hierarchies of stress-naïve mice, the subordinate, but not dominant, mice exhibit significantly greater avoidance of novel social targets. However, following exposure to CSDS, both lowest- and highest-ranked mice exhibit strong susceptibility to stress as measured by decreased interactions with a novel social target.These results suggest that the response to chronic social stress did not determine social rank in new cohorts, but low-status mice in newly established groups exhibited lower sociability to novel social targets. Interestingly, exposure of a hierarchical social group to chronic social stress led to stress-susceptibility in both high- and low-status mice as measured by social interaction.HighlightsStress susceptibility to chronic social defeat did not impede the establishment of dominance in new hierarchies.Subordinate mice exhibit reduced social preference after hierarchy formation.Following chronic social defeat stress, both subordinate and dominant mice exhibit susceptible-like reduction in social interaction, but dominant mice exhibit the greater decrease in social preference as compared to baseline.

scholarly journals Chronic Social Stress Impairs Prefrontal Cortical Myelination in Juvenile Mice

2020 ◽  
Author(s):  
Xuan Sun ◽  
Qiu-Hui-Hong Yu ◽  
Fei Luo ◽  
Bao-Ming Li
Keyword(s):  
Social Stress ◽  
Basic Protein ◽  
Social Defeat ◽  
Oligodendrocyte Precursor Cells ◽  
Potential Mechanism ◽  
Social Defeat Stress ◽  
Prefrontal Cortical ◽  
Chronic Social Defeat Stress ◽  
Oligodendrocyte Precursor ◽  
Medial Pfc

Abstract The prefrontal cortex (PFC) is a key brain region mediating many cognitive functions, and its structures and functions are particularly vulnerable to stress. Chronic social defeat stress (CSD) has been proposed as a model of anxiety/depressive-like behaviors. In the present study, we examined whether CSD affects the myelination in the medial PFC (mPFC) in mice. Our results show that CSD dramatically reduced the myelin basic protein (MBP) staining in the mPFC, with no effect on the MBP-labeling in the motor cortex, striatum, hippocampus and corpus callosum. Consistently, the CSD mice demonstrated a significant increase in oligodendrocyte precursor cells (PDGFRα+ cells) and a significant decrease in mature oligodendrocytes (CC1+/Olig2+ cells) in the mPFC. The present study demonstrates that CSD impairs the differentiation of oligodendrocytes and myelination in the mPFC, suggesting a potential mechanism for stress-induced change in PFC-dependent behaviors.

Chronic social defeat stress: Impacts on ethanol-induced stimulation, corticosterone response, and brain monoamine levels

2020 ◽  
Vol 34 (4) ◽  
pp. 412-419 ◽  
Author(s):  
Cristiane A Favoretto ◽  
Yasmin C Nunes ◽  
Giovana C Macedo ◽  
Janaína Silva Rocha Lopes ◽  
Isabel M Hartmann Quadros
Keyword(s):  
Frontal Cortex ◽  
Social Stress ◽  
Chronic Exposure ◽  
Social Defeat ◽  
Plasma Corticosterone ◽  
Social Defeat Stress ◽  
Brain Monoamines ◽  
Corticosterone Secretion ◽  
Chronic Social Defeat Stress ◽  
Brain Monoamine

Background: Chronic exposure to stress may dysregulate the hypothalamic-pituitary-adrenal axis and brain monoamine levels, contributing to the development of ethanol dependence. Exposure to chronic social defeat stress may impact ethanol-related effects, neural, and endocrine functions. Aim: This study assessed ethanol-induced locomotor activity, corticosterone responses, and brain monoamine levels in Swiss albino mice 10 days post-exposure to chronic social defeat stress. Methods: During a period of 10 days, male Swiss mice were exposed to daily defeat episodes, followed by housing with an aggressive mouse for 24 h. Control mice were housed in pairs and rotated every 24 h. Ten days post-stress, locomotor behavior was recorded after a challenge with ethanol (2.2 g/kg; intraperitoneal) or saline. After the test, blood and brain samples were collected for determination of plasma corticosterone and brain monoamines across different brain areas through high-performance liquid chromatography. Results: Defeated mice failed to show a stimulant locomotor response to ethanol, while controls displayed the expected ethanol-induced stimulation. Ethanol increased plasma corticosterone levels, with lower corticosterone secretion in defeated mice. Brain monoamines were affected by social defeat and ethanol, varying in different brain regions. Social stress reduced levels of dopamine, noradrenaline, and serotonin in the hypothalamus. Defeated mice presented reduced serotonin and dopamine levels in the frontal cortex. In the striatum, ethanol treatment increased dopamine levels in controls, but failed to do so in defeated mice. Conclusions: Our results suggest that chronic exposure to social defeat blunted ethanol-induced locomotor stimulation, and reduced ethanol-induced corticosterone secretion. Social stress promoted differential reductions in brain monoamine levels in the hypothalamus and frontal cortex and blunted ethanol-induced dopamine increases in the striatum.

scholarly journals Ingestion of probiotic (Lactobacillus helveticus and Bifidobacterium longum) alters intestinal microbial structure and behavioral expression following social defeat stress

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Katherine A. Partrick ◽  
Anna M. Rosenhauer ◽  
Jérémie Auger ◽  
Amanda R. Arnold ◽  
Nicole M. Ronczkowski ◽  
...  
Keyword(s):  
Social Stress ◽  
Bifidobacterium Longum ◽  
Social Defeat ◽  
Lactobacillus Helveticus ◽  
Rrna Gene ◽  
Social Avoidance ◽  
Social Defeat Stress ◽  
Microbial Structure ◽  
Microbial Composition ◽  
Anti Inflammatory

AbstractSocial stress exacerbates anxious and depressive behaviors in humans. Similarly, anxiety- and depressive-like behaviors are triggered by social stress in a variety of non-human animals. Here, we tested whether oral administration of the putative anxiolytic probiotic strains Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 reduces the striking increase in anxiety-like behavior and changes in gut microbiota observed following social defeat stress in Syrian hamsters. We administered the probiotic at two different doses for 21 days, and 16S rRNA gene amplicon sequencing revealed a shift in microbial structure following probiotic administration at both doses, independently of stress. Probiotic administration at either dose increased anti-inflammatory cytokines IL-4, IL-5, and IL-10 compared to placebo. Surprisingly, probiotic administration at the low dose, equivalent to the one used in humans, significantly increased social avoidance and decreased social interaction. This behavioral change was associated with a reduction in microbial richness in this group. Together, these results demonstrate that probiotic administration alters gut microbial composition and may promote an anti-inflammatory profile but that these changes may not promote reductions in behavioral responses to social stress.

scholarly journals Brain histamine and oleoylethanolamide restore behavioral deficits induced by chronic social defeat stress in mice

2021 ◽  
pp. 100317
Author(s):  
Barbara Rani ◽  
Andrea Santangelo ◽  
Adele Romano ◽  
Justyna Barbara Koczwara ◽  
Marzia Friuli ◽  
...  
Keyword(s):  
Social Defeat ◽  
Social Defeat Stress ◽  
Behavioral Deficits ◽  
Brain Histamine ◽  
Chronic Social Defeat Stress

scholarly journals Low-Molecular Weight BDNF Mimetic, Dimeric Dipeptide GSB-106, Reverses Depressive Symptoms in Mouse Chronic Social Defeat Stress

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 252
Author(s):  
Tatiana A. Gudasheva ◽  
Anna V. Tallerova ◽  
Armen G. Mezhlumyan ◽  
Tatyana A. Antipova ◽  
Ilya O. Logvinov ◽  
...  
Keyword(s):  
Dose Range ◽  
Social Defeat ◽  
Social Defeat Stress ◽  
In Vivo Experiments ◽  
Trk Receptor ◽  
Chronic Social Defeat Stress ◽  
Swimming Test ◽  
Scientific Group

A mimetic of the BDNF loop 4, bis (N-monosuccinyl-L-seryl-L-lysine) hexamethylenediamide, named GSB-106, was designed and synthesized in our scientific group. The compound activated TrkB, MAPK/ERK, PI3K/AKT, and PLCγ in in vitro experiments. In vivo experiments with rodents revealed its antidepressant-like activity in the forced swim and the tail suspension tests at the dose range of 0.1–5.0 mg/kg (i.p., p.o.). However, GSB-106 was not studied in depression models modulating major depression in humans. In the present study, the GSB-106 antidepressant-like activity was revealed in mice at the depression model induced by 28-day social defeat stress with 21-days oral administration (0.1 mg/kg) after stress. At the same time, GSB-106 restored reduced locomotor activity and completely eliminated the anhedonia manifestations. The compound also restored reduced levels of synaptophysin and CREB in the hippocampus. In addition, the Trk receptor antagonist K252A, and the PLC inhibitor U73122, were found to completely block the antidepressant-like activity of GSB-106 in the forced swimming test in mice. Thus, the present results demonstrate the dipeptide BDNF mimetic GSB-106 reversed depressive-like behavior and restored hippocampal neuroplasticity in a rodent depression model. These effects of GSB-106 are probably regulated by TrkB signaling.

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