Comparison of chronic physical and emotional social defeat stress effects on mesocorticolimbic circuit activation and voluntary consumption of morphine

Cooper, Sarah; Kechner, Megan; Caraballo-Pérez, D.; Kaska, Sophia; Robison, Alfred J.; Mazei-Robison, Michelle S.

doi:10.1038/s41598-017-09106-3

Cited by 34 publications

(38 citation statements)

References 50 publications

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“…S1b, c). Expanding upon our previous findings in the dHPC 21,22 , we found that ΔFosB was also induced in all subregions of the vHPC following repeated treatment with the antidepressant fluoxetine ( Fig. S1d, e), a selective serotonin reuptake inhibitor.…”

Section: Resultssupporting

confidence: 83%

“…It is also necessary in dorsal hippocampus (dHPC) for learning 17 , and regulates the excitability of dHPC CA1 neurons 18 as well as hippocampal neurogenesis 19,20 . ΔFosB is induced throughout HPC by stress and antidepressant treatment 13,[21][22][23] , and vHPC CA3 ΔFosB is critical for the prophylactic effects of ketamine on stress responses 23 . This indicates that ΔFosB is a critical modulator of vHPC function and may orchestrate long-term alterations in gene expression underlying depressive and anxiety disorders.…”

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confidence: 99%

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Circuit-specific hippocampal ΔFosB underlies resilience to stress-induced social avoidance

et al. 2020

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Chronic stress is a key risk factor for mood disorders like depression, but the stress-induced changes in brain circuit function and gene expression underlying depression symptoms are not completely understood, hindering development of novel treatments. Because of its projections to brain regions regulating reward and anxiety, the ventral hippocampus is uniquely poised to translate the experience of stress into altered brain function and pathological mood, though the cellular and molecular mechanisms of this process are not fully understood. Here, we use a novel method of circuit-specific gene editing to show that the transcription factor ΔFosB drives projection-specific activity of ventral hippocampus glutamatergic neurons causing behaviorally diverse responses to stress. We establish molecular, cellular, and circuit-level mechanisms for depression- and anxiety-like behavior in response to stress and use circuit-specific gene expression profiling to uncover novel downstream targets as potential sites of therapeutic intervention in depression.

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Section: Resultssupporting

confidence: 83%

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confidence: 99%

Circuit-specific hippocampal ΔFosB underlies resilience to stress-induced social avoidance

et al. 2020

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“…These findings parallel the effects of other stressors (e.g., footshock, tail-pinch), although it has been argued that physical stress modalities may, in part, engage endogenous opioid systems in response to minor injury, producing an increase in subsequent opioid-seeking or intake. A comparison between the effects of social defeat stress and the effects of a non-contact witness stress on morphine intake indicates that social threat may be sufficient to enhance the reinforcing effects of morphine, even in the absence of physical defeat ( Cooper et al, 2017 ). Yet, despite enduring changes in gene expression and neural activity, morphine preference is no longer apparent two weeks after stress exposure.…”

Section: Animal Models Of Social Stress and Pathological Patterns Of mentioning

confidence: 99%

Social defeat stress and escalation of cocaine and alcohol consumption: Focus on CRF

Newman

Leonard

Arena

et al. 2018

Neurobiology of Stress

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Both the ostensibly aversive effects of unpredictable episodes of social stress and the intensely rewarding effects of drugs of abuse activate the mesocorticolimbic dopamine systems. Significant neuroadaptations in interacting stress and reward neurocircuitry may underlie the striking connection between stress and substance use disorders. In rodent models, recurring intermittent exposure to social defeat stress appears to produce a distinct profile of neuroadaptations that translates most readily to the repercussions of social stress in humans. In the present review, preclinical rodent models of social defeat stress and subsequent alcohol, cocaine or opioid consumption are discussed with regard to: (1) the temporal pattern of social defeat stress, (2) male and female protocols of social stress-escalated drug consumption, and (3) the neuroplastic effects of social stress, which may contribute to escalated drug-taking. Neuroadaptations in corticotropin-releasing factor (CRF) and CRF modulation of monoamines in the ventral tegmental area and the bed nucleus of the stria terminalis are highlighted as potential mechanisms underlying stress-escalated drug consumption. However, the specific mechanisms that drive CRF-mediated increases in dopamine require additional investigation as do the stress-induced neuroadaptations that may contribute to the development of compulsive patterns of drug-taking.

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“…Rodents are reported to display various stress-related changes when directly witnessing SDS [5][6][7][8][9][10] . It has been suggested that they recognise the emotional state of conspecifics in distress as their own stress, using visual, auditory, and chemosensory stimuli as cues.…”

Section: Discussionmentioning

confidence: 99%

Indirect exposure to socially defeated conspecifics using recorded video activates the HPA axis and reduces reward sensitivity in mice

Nakatake

Furuie

Ukezono³

et al. 2020

Sci Rep

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Rodents perceive the emotional states of conspecifics using vision. In the present study, we demonstrated that exposure to the video-recorded distress of conspecifics induces stress responses in male C57BL/6J mice. A single exposure to a video-recorded scene of the social defeat stress (SDS) increased plasma corticosterone levels in these mice. This physiological change was suppressed by blocking the visual information, suggesting that vision plays a crucial role in inducing stress responses. Furthermore, after exposure to the video, there were increased numbers of c-Fos-positive neurons in the anterior cingulate cortex and other brain areas that are associated with the negative valence and empathy systems, but not in the regions related to the pain signaling. In addition, repeated exposure to SDS videos induced an apparent reduction in reward sensitivity in the sucrose preference test, but did not affect avoidance behaviour in the social interaction test or immobility behaviour in the forced swim test. Reduced reward sensitivity in mice reflects anhedonia, which is a core symptom of depression in humans. Our video SDS model therefore provides a unique opportunity to not only understand the mechanisms underlying stress-induced anhedonia, but also to screen effective candidate molecules for stress-related disorders with greater reproducibility.

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Comparison of chronic physical and emotional social defeat stress effects on mesocorticolimbic circuit activation and voluntary consumption of morphine

Cited by 34 publications

References 50 publications

Circuit-specific hippocampal ΔFosB underlies resilience to stress-induced social avoidance

Circuit-specific hippocampal ΔFosB underlies resilience to stress-induced social avoidance

Social defeat stress and escalation of cocaine and alcohol consumption: Focus on CRF

Indirect exposure to socially defeated conspecifics using recorded video activates the HPA axis and reduces reward sensitivity in mice

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