Convergent neuroendocrine mechanisms of social buffering and stress contagion

Abstract

Social interactions play a key role in modulating the impact of stressful experiences. In some cases, social interactions can result in social buffering, the process in which the presence of one individual reduces the physiological and behavioral impact of stress in another individual. On the other hand, there is growing evidence that a key initiating factor of social buffering behaviors is the initiation of an anxiogenic state in the individual that was not directly exposed to the stress. This is referred to as stress contagion (a form of emotion contagion). Both processes involve the transmission of social information, suggesting that contagion and buffering could share similar neural mechanisms. In general, mechanistic studies of contagion and buffering are considered separately, even though behavioral studies show that a degree of contagion is usually necessary for social buffering behaviors to occur. Here we consider the extent to which the neuropeptides corticotropin releasing hormone and oxytocin are involved in contagion and stress buffering. We also assess the importance that frontal cortical areas such as the anterior cingulate cortex and infralimbic cortex play in these behavioral processes. We suggest that further work that directly compares neural mechanisms during stress contagion and stress buffering will be important for identifying what appear to be distinct but overlapping circuits mediating these processes.

Keywords: Corticotropin releasing factor; Oxytocin; Paraventricular nucleus; Prefrontal cortex; Social defeat.

Figure 1:

Effects of cagemates on the impact of social defeat on social interaction behavior in male and female California mice. A) Experimental design. B) Effects of defeat on social approach to an unfamiliar, same-sex target mouse in males and females were stronger when focal mice were housed with at least one stressed cagemate. C) There were no differences in time spent interacting with an empty cage when the target mouse was absent. * p < 0.05 main effect of cagemate.

Figure 2:

Neuroendocrine mechanisms of social contagion and stress buffering. In demonstrators stress-exposure increases the sensitivity of CRH neurons to excitatory input and increased activation of CRHR1 receptors. Observers exposed to stressed demonstrators show a similar increase in CRH activity. Increased activity of oxytocin neurons results in the activation of OTR within the insular cortex to drive consolation related behaviors. These behaviors can blunt physiological stress responses and induce anxiolytic effects in demonstrators. At least some of these effects are mediated through the actions of oxytocin or activation of neurons within the infralimbic cortex. Currently it is unknown whether oxytocin acts specifically within the infralimbic cortex.