Social Defeat

Religion is positively correlated with subjective well-being across a variety of contexts, but convincing causal models are lacking. Some researchers have suggested that religion may boost self-control, and thus well-being, by requiring effortful rituals. This article proposes that costly signaling theory provides a vital explanatory tool for understanding these relationships. Signaling theories posit that religious adherents signal their commitment to religious collectives through difficult or anhedonic activities and rituals, creating a cost barrier for entry which protects religious communities against free riders. Because costly signaling behaviors require the inhibition of prepotent responses and intentional exposure to aversive stimuli, committed adherents build self-control over time. Subjective well-being is thus modeled as a longitudinal product of subjective investment in a religious social collective and the self-regulation abilities that emerge from signaling that investment. This emphasis on a feedback cycle driven by social signaling represents a novel contribution to investigations of religion and well-being. New longitudinal research in social investment theory and self-control lends the model conceptual credibility.

Rationale. Excessive alcohol (EtOH) drinking is difficult to
model in animals despite the extensive human literature demonstrating that stress increases EtOH consumption.
Objective. The current experiments show escalations in voluntary
EtOH drinking caused by a history of social defeat stress
and intermittent access to EtOH in C57BL/6J mice compared
to non-stressed mice given intermittent EtOH or continuous
EtOH. To explore a mechanistic link between stress and drinking,
we studied the role of corticotropin-releasing factor type-
1 receptors (CRF-R1) in the dopamine-rich ventral tegmental
area (VTA).
Results. Intra-VTA infusions of a CRF-R1 antagonist,
CP376395, infused into the VTA dose-dependently and selectively reduced intermittent EtOH intake in stressed and nonstressed mice, but not in mice given continuous EtOH. In
contrast, intra-VTA infusions of the CRF-R2 antagonist
astressin2B non-specifically suppressed both EtOH and H2O
drinking in the stressed group without effects in the nonstressed mice. Using in vivo microdialysis in the nucleus accumbens (NAc) shell, we observed that stressed mice drinking
EtOH intermittently had elevated levels of tonic dopamine
concentrations compared to non-stressed drinking mice.
Also, VTA CP376395 potentiated dopamine output to the
NAc only in the stressed group causing further elevations of
dopamine post-infusion.
Conclusions. These findings illustrate a role for
extrahypothalamic CRF-R1 as especially important for
stress-escalated EtOH drinking beyond schedule-escalated
EtOH drinking. CRF-R1 may be a mechanism for balancing
the dysregulation of stress and reward in alcohol use disorders.

A major impediment to novel drug development has been the paucity of animal models that accurately reflect symptoms of affective disorders. In animal models, prolonged social stress has proven to be useful in understanding the molecular mechanisms underlying affective-like disorders. When considering experimental approaches for studying depression, social defeat stress, in particular, has been shown to have excellent etiological, predictive, discriminative and face validity. Described here is a protocol whereby C57BL/6J mice that are repeatedly subjected to bouts of social defeat by a larger and aggressive CD-1 mouse results in the development of a clear depressive-like syndrome, characterized by enduring deficits in social interactions. Specifically, the protocol consists of three important stages, beginning with the selection of aggressive CD-1 mice, followed by agonistic social confrontations between the CD-1 and C57BL/6J mice, and concluding with the confirmation of social avoidance in subordinate C57BL/6J mice. The automated detection of social avoidance allows a marked increase in throughput, reproducibility and quantitative analysis. This protocol is highly adaptable, but in its most common form it requires 3–4 weeks for completion.