Defeat stress in rodents: From behavior to molecules

Hammels, Caroline; Pishva, Ehsan; Vry, Jochen De; Hove, Daniël L.A. van den; Prickaerts, Jos; Winkel, Ruud van; Selten, Jean‐Paul; Lesch, Klaus‐Peter; Daskalakis, Nikolaos P.; Steinbusch, Harry W.M.; Os, Jim van; Kenis, Günter; Rutten, Bart P. F.

doi:10.1016/j.neubiorev.2015.10.006

Cited by 192 publications

(125 citation statements)

References 219 publications

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“…One key feature of the resident-intruder paradigm is that it can produce depressive-like behaviors in rodents (Gomez-Lazaro et al, 2011; Hammels et al, 2015; Perez-Tejada et al, 2013; Wood et al, 2010; Wood et al, 2015). In agreement with our previous studies, active coping during social defeat was characterized by greater time in upright postures, increased defeat latencies and resiliency to the negative behavioral consequences of social stress as indicated by intact hedonic behavior in the sucrose preference test following stress (Wood et al, 2010; Wood et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

The protective effects of resveratrol on social stress-induced cytokine release and depressive-like behavior

Finnell

Lombard

Melson

et al. 2017

Brain, Behavior, and Immunity

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Social stress is a risk factor for psychiatric disorders, however only a subset of the population is susceptible while others remain resilient. Inflammation has been linked to the pathogenesis of psychosocial disorders in humans and may underlie these individual differences. Using a resident-intruder paradigm capable of revealing individual differences in coping behavior and inflammatory responses, the present study determined if resveratrol (RSV; 0, 10, 30mg/kg/day) protected against persistent stress-induced inflammation in socially defeated rats. Furthermore, the antidepressant efficacy of RSV was evaluated using the sucrose preference test. Active coping rats were characterized by more time spent in upright postures and increased defeat latencies versus passive coping rats. Five days after defeat, flow cytometry revealed enhanced stimulation of inflammatory proteins (IL-β, TNF-α) in spleen cells of passive rats as compared to active coping and controls, an effect that was blocked by both doses of RSV. Furthermore, only passive coping rats exhibited increased proinflammatory proteins (IL-1β, TNF-α, GM-CSF) in the locus coeruleus (LC), a noradrenergic brain region implicated in depression. Notably, only 30mg/kg RSV blocked LC neuroinflammation and importantly, was the only dose that blocked anhedonia. Alternatively, while stress had minimal impact on resting cytokines in the dorsal raphe (DR), RSV dose-dependently reduced DR cytokine expression. However, this did not result in changes in indoleamine 2,3-dioxygenase activity or serotonin levels. Taken together, these data suggest that social stress-induced depressive-like behavior evident in passive coping rats may be driven by stress-induced neuroinflammation and highlight natural anti-inflammatory agents to protect against social stress-related consequences.

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Section: Discussionmentioning

confidence: 99%

The protective effects of resveratrol on social stress-induced cytokine release and depressive-like behavior

Finnell

Lombard

Melson

et al. 2017

Brain, Behavior, and Immunity

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“…Thus, to have construct validity, an animal model must in the least utilize a life-threatening stressor. Some rodent models of PTSD, such as predator exposure and resident-intruder (social defeat) paradigms, may ascertain construct validity due to the naturalistic stressors (Burgado et al, 2014; Gautam et al, 2015; Hammels et al, 2015; Muhie et al, 2015; Wilson et al, 2014a; Zoladz et al, 2012; Zoladz et al, 2015). However, other models such as prolonged immobilization may fall short due to the artificial nature and duration of the stressor.…”

Section: Delineating the Relationships: Insight From Animal Modelsmentioning

confidence: 99%

Posttraumatic stress disorder: A metabolic disorder in disguise?

Michopoulos

Vester

Neigh

2016

Experimental Neurology

104

103

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Posttraumatic stress disorder (PTSD) is a heterogeneous psychiatric disorder that affects individuals exposed to trauma and is highly co-morbid with other adverse health outcomes, including cardiovascular disease and obesity. The unique pathophysiological feature of PTSD is the inability to inhibit fear responses, such that individuals suffering from PTSD re-experience traumatic memories and are unable to control psychophysiological responses to trauma-associated stimuli. However, underlying alterations in sympathetic nervous system activity, neuroendocrine systems, and metabolism associated with PTSD are similar to those present in traditional metabolic disorders, such as obesity and diabetes. The current review highlights existing clinical, translational, and preclinical data that support the notion that underneath the primary indication of impaired fear inhibition, PTSD is itself also a metabolic disorder and proposes altered function of inflammatory responses as a common underlying mechanism. The therapeutic implications of treating PTSD as a whole-body condition are significant, as targeting any underlying biological system whose activity is altered in both PTSD and metabolic disorders, (i.e. HPA axis, sympathetic nervous systems, inflammation) may elicit symptomatic relief in individuals suffering from these whole-body adverse outcomes.

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“…42,43 Lack of neutrophil support and impaired neuronal vascular supply have been offered as explanations. 44 Interestingly, several postmortem studies have described decreased numbers of hippocampal neurons in schizophrenia patients. 45 Taken together, these results indicate that it is important to examine whether social exclusion contributes to the development of the anatomic changes already present at the time of the first psychotic episode.…”

Section: Abnormal Neurodevelopmentmentioning

confidence: 99%

Biological Mechanisms Whereby Social Exclusion May Contribute to the Etiology of Psychosis: A Narrative Review

Selten

Booij

Buwalda

et al. 2017

SCHBUL

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The purpose of this review is to examine whether a contribution of social exclusion to the pathogenesis of psychosis is compatible with the dopamine hypothesis and/or the neurodevelopmental hypothesis. Humans experience social exclusion as defeating. An animal model for defeat is the resident-intruder paradigm. The defeated animal shows evidence of an increased sensitivity to amphetamine, increased dopamine release in the nucleus accumbens and prefrontal cortex, and increased firing of dopaminergic neurons in the ventral tegmental area. As for humans, one study showed that amphetamine-induced striatal dopamine release was significantly greater among nonpsychotic young adults with severe hearing impairment than among normal hearing controls. Two other studies reported an association between childhood trauma and increased dopamine function in striatal subregions. Several studies have suggested that the perigenual anterior cingulate cortex (pgACC) may play a role in the processing of social stress. Importantly, the pgACC regulates the activity of the ventral striatum through bidirectional interconnections. We are not aware of studies in humans that examined whether (proxies for) social exclusion contributes to the structural brain changes present at psychosis onset. Animal studies, however, reported that long-term isolation may lead to reductions in volume of the total brain, hippocampus, or medial prefrontal cortex. Other animal studies reported that social defeat can reduce neurogenesis. In conclusion, the answer to the question as to whether there are plausible mechanisms whereby social exclusion can contribute to the pathogenesis of psychosis is cautiously affirmative.

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Defeat stress in rodents: From behavior to molecules

Cited by 192 publications

References 219 publications

The protective effects of resveratrol on social stress-induced cytokine release and depressive-like behavior

The protective effects of resveratrol on social stress-induced cytokine release and depressive-like behavior

Posttraumatic stress disorder: A metabolic disorder in disguise?

Biological Mechanisms Whereby Social Exclusion May Contribute to the Etiology of Psychosis: A Narrative Review

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