Effects Of Social Stress Research Articles

Ethologically relevant repeated acute social stress induces maternal neglect in the lactating female mouse.

Psychosocial stress is a top predictor of peripartum mood disorders in human mothers. In the present study, we developed a novel paradigm testing the effects of direct and vicarious social stress on maternal and mood-related behaviors in B6 mice. Using a novel housing paradigm, we examined the extent to which postpartum dams withdrew from litters following psychosocial stress. Repeated acute direct social stress involved exposing dams to a virgin male mouse for 7min/day on postpartum days 5-7 during a brief (15-min) mother-pup separation. To remove the effects of direct stress, the vicarious social stress dams were housed in the same vivarium as direct social stressed dams, but without direct exposure to intruders. Control dams were given mock intruder exposure and housed in a separate vivarium room containing breeding mice. All dams experienced pup separation, and maternal care was investigated upon reunion. Direct and vicarious social stress induced significant deficits in maternal care and increased maternal anxiety relative to controls. Although vicarious stress effects were more likely to occur on days when there was acute stress exposure, direct stress sustained maternal deficits 24h after the final stressor. Together, these data suggest psychosocial stress induces aberrant maternal phenotypes in mice.

Examining the interplay of emotion regulation strategies, social stress, and gender in predicting life satisfaction of emerging adults

Previous research has consistently shown the importance of emotion regulation in human development, but little work has investigated the synergistic effects of dispositional and situational factors on how emotion regulation works. Guided by a recent framework that proposes emotion regulation as a combination of person, situation, and strategy (Doré, Silvers, & Ochsner, 2016), this study examined the three-way interaction effects of gender (male, female), social stress (low, moderate, high levels), and emotion regulation strategies (reappraisal, suppression) on life satisfaction in emerging adults. Using self-report survey data (n = 353), significant three-way interaction effects were found. Specifically, positive association between cognitive reappraisal and life satisfaction was significant for both genders across all stress levels, except at low stress level for males. As the stress level increased, the magnitude of such association decreased for females but increased for males. In contrast, the association between expressive suppression and life satisfaction was not significant for both genders across all stress levels, except at high stress level for males where suppression had a significant positive relation with life satisfaction. Findings demonstrated the differential effects of reappraisal and suppression on life satisfaction across gender and social stress levels.

Fluoxetine and environmental enrichment similarly reverse chronic social stress-related depression- and anxiety-like behavior, but have differential effects on amygdala gene expression

The adverse effects of stress on brain and behavior have long been known and well-studied, with abundant evidence linking stress to, among other things, mood and anxiety disorders. Likewise, many have investigated potential treatments for stress-related mood and anxiety phenotypes and demonstrated good response to standard antidepressant medications like selective serotonin reuptake inhibitors (SSRIs), as well as environmental manipulations like exercise or enrichment. However, the extent to which stress and various treatments act on overlapping pathways in the brain is less well understood. Here, we used a widely studied social defeat stress paradigm to induce a robust depression- and anxiety-like phenotype and chronic corticosterone elevation that persisted for at least 4 weeks in wild type male mice. When mice were treated with either the SSRI fluoxetine or an enriched environment, both led to similar behavioral recovery from social defeat. We then focused on the amygdala and assessed the effects of social defeat, fluoxetine, and enrichment on 168 genes broadly related to synaptic plasticity or oxidative stress. We found 24 differentially expressed genes in response to social defeat stress. Interestingly, fluoxetine led to broad normalization of the stress-induced expression pattern while enrichment led to expression changes in a separate set of genes. Together, this study provides additional insight into the chronic effects of social defeat stress on behavior and gene expression in the amygdala. The findings also suggest that, for a subset of genes assessed, fluoxetine and environmental enrichment have strikingly divergent effects on expression in the amygdala, despite leading to similar behavioral outcomes.

Decreased kynurenine pathway potentiate resilience to social defeat effect on cocaine reward

The kynurenine (KYN) pathway of tryptophan (TRP) degradation is activated by stress and inflammatory factors. It is now well established that social stress induces the activation of the immune system, with central inflammation and KYN metabolism being two of the main factors linking stress with depression.The aim of the present study was to evaluate the long-lasting changes in the KYN pathway induced by social defeat (SD) associated with the resilience or susceptibility to an increase in the conditioned rewarding effects of cocaine. Mice were exposed to repeated SD and 3 weeks later, a conditioned place preference (CPP) induced by a subthreshold dose of cocaine (1.5 mg/kg) was developed. KYN levels in plasma, cerebellum, hippocampus, striatum and limbic forebrain were studied at the end of the CPP procedure. Changes in the KYN pathway after exposure to pharmacological (oxytocin and indomethacin) and environmental interventions (environmental enrichment) were also evaluated.Our results showed that defeated susceptible (SD-S) mice had higher conditioning scores than resilient mice (SD-R). In addition, although KYN concentration was elevated in all defeated mice, SD-R mice showed smaller increases in KYN concentration in the cerebellum than SD-S mice. Oxytocin or Indomethacin treatment before SD normalized cocaine-induced CPP, although the increase in the KYN pathway was maintained. However, environmental enrichment before SD normalized cocaine-induced CPP and prevented the increase in the KYN pathway.The present study highlights the role of the KYN pathway and anti-inflammatory drugs acting on TRP metabolism as pharmacological targets to potentiate resilience to social stress effects.

Through Her Eyes: The Impact of War on Syrian Refugee Families.

The Syrian war conflict ended with devastating impact on Syrian refugee women and their children. A few studies have been done that explored the impact of the civil war and displacement of Syrian families from a cultural perspective. The purpose of this study was to highlight the experiences of the Syrian war-refugee families who have sought shelter in a host country. A descriptive phenomenological study was conducted using a semistructured interview approach among 16 Syrian refugee women who were approached from two Jordanian health care centers. The main themes discussed how the war ended with financial and social stress, family violence, and hazardous effects on women and children health. This article introduced how culture and religion influence how family unit and members responded to war stressors. This study provided transcultural nursing knowledge, allowing nurses to be grounded in individualized culturally specific care.

Long-term effects of stress resilience: Hippocampal neuroinflammation and behavioral approach in male rats.

Resilience to stress is the ability to quickly adapt to adversity. There is evidence that exposure to prolonged stress triggers neuroinflammation what produces individual differences in stress vulnerability. However, the relationship between stress resilience, neuroinflammation, and depressive-like behaviors remains unknown. The aim of this study was to analyze the long-term effects of social defeat stress (SDS) on neuroinflammation in the hippocampus and depressive-like behaviors. Male rats were subjected to the SDS paradigm. Social interaction was analyzed 1 and 2weeks after ending the SDS to determine which animals were susceptible or resilient to stress. Neuroinflammation markers glial fibrillary acidic protein, ionized calcium-binding adaptor molecule 1, and elevated membrane permeability in astrocytes and microglia, as well as depressive-like behaviors in the sucrose preference test and forced swim test were evaluated in all rats. One week after SDS, resilient rats increased their sucrose preference, and time spent in the floating behavior decreased in the forced swim test compared to susceptible rats. Surprisingly, resilient rats became susceptible to stress, and presented neuroinflammation 2weeks after SDS. These findings suggest that SDS-induced hippocampal neuroinflammation persists in post-stress stages, regardless of whether rats were initially resilient or not. Our study opens a new approach to understanding the neurobiology of stress resilience.

Social status and previous experience in the group as predictors of welfare of sows housed in large semi-static groups.

Mixing gestating sows implies hierarchy formation and has detrimental consequences on welfare. The effects of social stress on the most vulnerable individuals may be underestimated and it is therefore important to evaluate welfare between individuals within groups. This study aimed at investigating the impact of social status and previous experience in the group on well-being of sows housed in large semi-static groups. We assessed aggression (d0 (mixing), d2, d27, d29), body lesions (d1, d26, d84) and feeding order on 20 groups of 46–91 animals. Social status was based on the proportion of fights won during a 6-hr observation period between d0 and d2. Dominants (29%) were those who won more fights than they lost, Subdominants (25%) won fewer fights than they lost, Losers (23%) never won any fight in which they were involved while Avoiders (23%) were never involved in fights. Resident sows (70%) were already present in the group in the previous gestation while New sows (30%) were newly introduced at mixing. Subdominants and Dominants were highly involved in fights around mixing but this was more detrimental for Subdominants than Dominants, Losers and Avoiders since they had the highest body lesion scores at mixing. Avoiders received less non-reciprocal agonistic acts than Losers on d2 (P = 0.0001) and had the lowest body lesion scores after mixing. However, Avoiders and Losers were more at risk in the long-term since they had the highest body lesions scores at d26 and d84. They were followed by Subdominants and then Dominants. New sows fought more (P<0.0001), tended to be involved in longer fights (P = 0.075) around mixing and had more body lesions throughout gestation than Resident sows. Feeding order from one-month post-mixing was influenced both by the previous experience in the group and social status (P<0.0001). New sows, especially with a low social status, are more vulnerable throughout gestation and could serve as indicators of non-optimal conditions.

Effects of Social Support Toward Working Stress of The Nurses of X Hospital

Nurse has essential role to provide health care for public. When the nurse has demands of work more increasing, it causes arising stress. This study aims to find out the effects of social support toward work stress. This study is conducted to the 30 intensive care ICU and ICCU nurses who is consisted of 11 males and 19 females. As a result, the calculation result indicates that p-value 0.006 < 0.05 so that it can be inferred that the effects of social support of work stress toward work stress of nurses in X hospital.

A LATE MESOLITHIC FORAGER DISPERSAL CAUSED PRE‐AGRICULTURAL DEMOGRAPHIC TRANSITION IN NORWAY

SummaryPopulation growth has always played a key role in human mobility, even before the age of farming and husbandry. This paper explores population dynamics among early Holocene (∼9500–1700 cal BCE) hunter‐fisher‐gatherers in Southern Norway, focusing in particular on the Mesolithic‐Neolithic transition (4000/3900 cal BCE). Radiocarbon dates are calibrated and turned into summed probability distributions (SPDs). A heuristic linear method is used to calculate annual growth rates from the SPDs. Observed fluctuations in the SPDs are tested for significance by applying a Monte Carlo‐based simulation method. The paper finds evidence of a steady growth rate from the Boreal period until a sudden population trough at ∼4330–4300 cal BCE. The trough coincides with indications from the archaeological record of a dispersal of hunter‐fisher‐gatherers from Southern Scandinavia to Norway. The dispersal was likely an effect of lowered habitat suitability and social stress caused by population pressure among Southern Scandinavian hunter‐fisher‐gatherers. In Southern Norway, the proxy data show that the trough enabled a subsequent ‘boom’ in population and the emergence of regional technological innovations that define the Mesolithic‐Neolithic transition.

Effects of acute stress on probabilistic reversal learning in healthy participants

IntroductionAltered reward-based learning and stress play an important role in psychiatric illnesses, such as psychosis or addiction. Stress sometimes increases learning from rewards, other times it does not show an effect (Starcke &amp; Brand, 2016). A task addressing reward-based learning is the reversal learning task, which uses probabilistic rewards as feedback and incorporates sudden changes in reward contingencies. The effects of acute stress on reversal learning have rarely been addressed.ObjectivesHere, we investigated the effect of acute social stress in a within-subject design in healthy participants.MethodsA sample of n = 28 male non-clinical participants performed the task in a control condition versus the Trier Social Stress Test (TSST), a validated method to induce psychosocial stress. In our version of the reversal learning task (Reiter, 2016), participants choose between two anti-correlated stimuli in order to obtain rewards in three blocks. Reward contingencies remain stable for the first 55 trials and the last 35 trials. During the second block, in between the stable blocks, four changes of reward contingencies require participants to flexibly adapt their behavior. Performance was measured in correct responses, switches after losses and wins.ResultsCortisol and subjective stress responses showed that the stress induction was successful. Preliminary analyses showed no significant effect of stress induction on any of the performance measures.ConclusionsThese results demonstrate that reversal learning, at least regarding overall performance measures in our task, is robust to stress-related changes. Modeling and fMRI analyses could yield further insights into more subtle changes after stress induction.DisclosureNo significant relationships.

Neural circuits and activity dynamics underlying sex-specific effects of chronic social isolation stress

Exposure to prolonged stress in critical developmental periods induces heightened vulnerability to psychiatric disorders, which may have sex-specific consequences. Here we investigate the neuronal circuits mediating behavioral changes in mice after chronic adolescent social isolation stress. Escalated aggression is exhibited in stressed males, while social withdrawal is shown in stressed females. Invivo multichannel recordings of free-moving animals indicate that pyramidal neurons in prefrontal cortex (PFC) from stressed males exhibit the significantly decreased spike activity during aggressive attacks, while PFC pyramidal neurons from stressed females show a blunted increase of discharge rates during sociability tests. Chemogenetic and electrophysiological evidence shows that PFC hypofunctioning and BLA principal neuron hyperactivity contribute to the elevated aggression in stressed males, while PFC hypofunctioning and VTA dopamine neuron hypoactivity contribute to the diminished sociability in stressed females. These results establish a framework for understanding the circuit and physiological mechanisms underlying sex-specific divergent effects of stress.

Unique effects of social defeat stress in adolescent male mice on the Netrin-1/DCC pathway, prefrontal cortex dopamine and cognition (Social stress in adolescent vs. adult male mice).

For some individuals, social stress is a risk factor for psychiatric disorders characterized by adolescent onset, prefrontal cortex (PFC) dysfunction and cognitive impairments. Social stress may be particularly harmful during adolescence when dopamine (DA) axons are still growing to the PFC, rendering them sensitive to environmental influences. The guidance cue Netrin-1 and its receptor, DCC, coordinate to control mesocorticolimbic DA axon targeting and growth during this age. Here, we adapted the accelerated social defeat (AcSD) paradigm to expose male mice to social stress in either adolescence or adulthood and categorized them as “resilient” or “susceptible” based on social avoidance behavior. We examined whether stress would alter the expression of DCC and Netrin-1 in mesolimbic DA regions and would have enduring consequences on PFC DA connectivity and cognition. While in adolescence the majority of mice are resilient but exhibit risk-taking behavior, AcSD in adulthood leads to a majority of susceptible mice without altering anxiety-like traits. In adolescent, but not adult mice, AcSD dysregulates DCC and Netrin-1 expression in mesolimbic DA regions. These molecular changes in adolescent mice are accompanied by changes in PFC DA connectivity. Following AcSD in adulthood, cognitive function remains unaffected, but all mice exposed to AcSD in adolescence show deficits in inhibitory control when they reach adulthood. These findings indicate that exposure to AcSD in adolescence versus adulthood has substantially different effects on brain and behavior and that stress-induced social avoidance in adolescence does not predict vulnerability to deficits in cognitive performance.

Battery Discharge from Monday to Friday: Background Social Stress at Work is Associated with more Rapid Accumulation of Fatigue

PurposeThis field study investigated the effects of background social stress at work on the weekly course of evening fatigue.MethodsMale employees of a Swiss organisation reported their fatigue after work and at 9 pm in the evening over three weeks. A total of 482 evening fatigue measurements from 34 male participants were subjected to multilevel analysis.ResultsSleep quality in the previous night and fatigue after work predicted evening fatigue. Evening fatigue was not associated with the time spent on daily housework or child care. There was a linear increase in evening fatigue across weekdays and a main effect of workplace social stressors on evening fatigue. Sleep quality during the previous night mediated the link between background social stressors and evening fatigue. Moreover, an interaction between workplace social stressors and working days indicated that fatigue accumulated faster during the working week in those reporting a high level of social stress at work.ConclusionSocial stress at work seems to accelerate the loss of resources over consecutive workdays. The analysis of workplace social stressors and other potential moderators of resource dynamics contributes to our understanding of work-related stress, including the role of background stressors and the temporal dynamics of resource loss.

Region- and receptor-specific effects of chronic social stress on the central serotonergic system in mice.

Serotonin (5-HT), via its receptors expressed in discrete brain regions, modulates aversion and reward processing and is implicated in various psychiatric disorders including depression. Stressful experiences affect central serotonergic activity and act as a risk factor for depression; this can be modelled preclinically. In adult male C57BL/6J mice, 15-day chronic social stress (CSS) leads to depression-relevant behavioural states, including increased aversion and reduced reward sensitivity. Based on this evidence, here we investigated CSS effects on 5-HT1A, 5-HT2A, and 5-HT2C receptor binding in discrete brain regions using in vitro quantitative autoradiography with selective radioligands. In addition, mRNA expression of Htr1a, 2a, 2c and Slc6a4 (5-HT transporter) was measured by quantitative PCR. Relative to controls, the following effects were observed in CSS mice: 5-HT1A receptor binding was markedly increased in the dorsal raphe nucleus (136%); Htr1a mRNA expression was increased in raphe nuclei (19%), medial prefrontal cortex (35%), and hypothalamic para- and periventricular nuclei (21%) and ventral medial nucleus (38%). 5-HT2A receptor binding was decreased in the amygdala (48%) and ventral tegmental area (60%); Htr2a mRNA expression was increased in the baso-lateral amygdala (116%). 5-HT2C receptor binding was decreased in the dorsal raphe nucleus (42%). Slc6a4 mRNA expression was increased in the raphe (59%). The present findings add to the translational evidence that chronic social stress impacts on the central serotonergic system in a region- and receptor-specific manner, and that this altered state of the serotonergic system contributes to stress-induced dysfunctions in emotional processing.

Density-dependence of nestling immune function and physiological condition in semi-precocial colonial bird: a cross-fostering experiment

BackgroundNesting in large aggregations provides several important advantages for colonially breeding birds. However, it also imposes certain costs, associated with facilitated pathogen transmission and social stress. The cost-benefit ratio is not similar for all the birds in a colony and it might be mediated by nest density. To investigate the influence of nest density on cell-mediated immune function and on physiological condition of nestlings, we arranged a cross-fostering experiment in three breeding colonies of black-headed gulls Chroicocephalus ridibundus. First, we exchanged eggs between plots of high and low nest density. Afterwards, we performed phytohaemagglutinin (PHA) skin test and we measured blood haemoglobin concentration in nearly 350 nestlings from experimental (exchanged) and control (non-exchanged) groups.ResultsWe found that PHA response was lowest in high nest density control group, indicating that depressed immune function of offspring, likely caused by social stress, can be considered as a cost of colonial breeding. Contrastingly, body condition of nestlings was the poorest in low density control group.ConclusionNestlings hatched and raised in high nest density plots did not have higher blood haemoglobin concentration in comparison to other study groups. Furthermore, they were affected with depressed cell mediated immune function, which is possibly driven by combined maternal (corticosteroid hormones deposited in yolk) and environmental (elevated social stress) effects. These results indicate that breeders from high nest densities do not benefit by rising offspring in better quality, in terms of immune function and body condition, although, in the light of previous studies, high nest densities are occupied by birds of higher individual quality, than low density areas. Our study provides a novel insight into the mechanisms of density-dependence that govern fitness of colonially nesting birds.

Social isolation stress facilitates chemically induced oral carcinogenesis.

Social isolation has affected a large number of people and may lead to impairment of physical and mental health. Although stress resulting from social isolation may increase cancer progression, its interference on tumorigenesis is poorly known. In this study, we used a preclinical model to evaluate the effects of social isolation stress on chemically induced oral carcinogenesis. Sixty-two 21-day-old male Wistar rats were divided into isolated and grouped groups. After 90 days of age, the rats from both groups underwent oral carcinogenesis with 4-nitroquinoline 1-oxide (4NQO) for 20 weeks. All rats were assessed for depressive-like behavior and euthanized for oral squamous cell carcinoma (OSCC) diagnosis and measurement of inflammatory mediators in the tumor microenvironment. Social isolation stress increased the OSCC occurrence by 20.4% when compared to control. Isolated rats also showed higher tumor volume and cachexia than the grouped rats. Social isolation did not induce changes in the depressive-like behavior after carcinogenic induction. Tumors from stressed rats had increased levels of the inflammatory mediators, TNF-alpha, IL1-beta and MCP-1. The concentrations of TNF-alpha and MCP-1 were significantly increased in the large tumors from isolated animals. Higher tumor levels of TNF-alpha, IL-6, IL1-beta and MCP-1 were positively correlated with OSCC growth. This study provides the first evidence that social isolation stress may facilitate OSCC occurrence and tumor progression, an event accompanied by increased local levels of inflammatory mediators.

The Effects of Chronic Social Defeat Stress on Solid Gastric Emptying and Defecation in C57BL/6J Mice

Stress contributes to mental disorders as well as functional gastrointestinal disorders. In functional gastrointestinal disorders, gastrointestinal motility is thought to play a role. Therefore, we evaluated the effects of chronic social defeat stress on gastrointestinal motility in C57BL/6J mice, by measuring gastric emptying, fecal pellet output, and gastrointestinal transit. In mice subjected to 10 days of social defeat stress, serum corticosterone concentrations were significantly higher, relative tissue weights of spleen and adrenal gland tissues were significantly heavier, and thymus sizes were smaller than in the control mice. Stressed mice exhibited social avoidance behavior in a social interaction test and anxiety-like behavior and lower locomotor activity in an elevated plus maze test. In gastric emptying test, stressed mice displayed increased gastric emptying rate with significant suppression of short-time (30 min.) test diet intake. Fecal pellet output and gastrointestinal transit were not different in control and stressed mice. These results suggest that chronic social defeat stress influences gastric motility. Thus, the social defeat stress model may be useful for studying psychiatric disease and functional gastrointestinal disorders simultaneously.

Interaction Between Social Defeat Stress and Chronic Ethanol Exposure on Behaviors During Ethanol Withdrawal and Pro-Inflammatory Cytokines in Mice

Stress and ethanol consumption are known to affect the immune system, interfering in individual health, and resistance to opportunistic diseases. When experienced together, stress and ethanol seem to interact uniquely, altering each other effects depending on the exposure schedule. However, the effects of social stress on chronic ethanol exposure effects on the immune system are not well elucidated. To study this interaction, we chronically treated male swiss mice with ethanol after repeated social defeat stress (SDS) exposure. Some animals were tested in the elevated plus-maze (EPM) and open field (OF) while another cohort had plasmatic TNF-α, TGF-β1, CXCL-1, CCL-2, and VEGF quantified. Mice exposed to SDS or ethanol withdrawal showed increased anxiety-like behaviors in the EPM, while ethanol withdrawal decreased locomotor activity. Both alterations were attenuated in the groups exposed to SDS and ethanol withdrawal. Ethanol and stress alone increased plasmatic CXCL-1, while only stress affected CCL-2 and VEGF. Our results suggest that SDS exposure and ethanol withdrawal attenuated the increase in anxiety-like behaviors, but did not alter each other effects on cytokine content.

Neurobiological Bases of Alcohol Consumption After Social Stress.

The urge to seek and consume excessive alcohol is intensified by prior experiences with social stress, and this cascade can be modeled under systematically controlled laboratory conditions in rodents and non-human primates. Adaptive coping with intermittent episodes of social defeat stress often transitions to maladaptive responses to traumatic continuous stress, and alcohol consumption may become part of coping responses. At the circuit level, the neural pathways subserving stress coping intersect with those for alcohol consumption. Increasingly discrete regions and connections within the prefrontal cortex, the ventral and dorsal striatum, thalamic and hypothalamic nuclei, tegmental areas as well as brain stem structures begin to be identified as critical for reacting to and coping with social stress while seeking and consuming alcohol. Several candidate molecules that modulate signals within these neural connections have been targeted in order to reduce excessive drinking and relapse. In spite of some early clinical failures, neuropeptides such as CRF, opioids, or oxytocin continue to be examined for their role in attenuating stress-escalated drinking. Recent work has focused on neural sites of action for peptides and steroids, most likely in neuroinflammatory processes as a result of interactive effects of episodic social stress and excessive alcohol seeking and drinking.

Post-Acute Sequelae of COVID-19 (PASC): Association with Inflammation and Autoimmunity

It has become increasingly evident that a high percentage of patients that recover from acute COVID-19 infection continue to suffer from a variety of persistent symptoms even months after viral clearance, the most common ones being fatigue, dyspnea, anosmia, dysgeusia, cognitive dysfunction, and psychological problems, including anxiety and depression. This syndrome, known as Post-acute sequelae of COVID-19 (PASC), can severely affect the life quality and represents an important health care concern. The exact causes for the symptoms observed in patients with PASC remain to be adequately characterized, but are likely to be associated with multiple factors, including residual disease and/or inflammation, organ damage, effects of hospitalization and/or prolonged ventilation, as well as effects of social isolation and stress. This mini-review discusses evidence that may link both inflammatory and auto-immune processes in the pathophysiology of PASC.