Translational Implications of Oxytocin-Mediated Social Buffering Following Immobilization Stress in Female Prairie Voles

Abstract

The supportive interpersonal social network resources available to individuals to provide help and assistance in times of need are one of the most studied aspects of resilience and recuperation in trauma research (1). Both the perceived availability and the objective presence of social support moderate the relationship between stress, stress response, and stress-induced psychopathology (1). A more recent report indicated that unstable family and social relationships impair coping and rehabilitation after trauma (2). Two meta-analysis studies of the predictors of posttraumatic stress disorder (PTSD) in adults likewise confirmed that the lack of social support is one of the most important risk factors for posttraumatic stress reactions (3,4). Social support protects against various adverse physical and mental disorders (e.g., cardiovascular reactivity, metabolic syndromes, and hypertension and depression and schizophrenia) (1). However, despite such accumulating evidence, the precise neurobiological mechanisms mediating the positive effects of social contact and social interactions on stress-responsive physiologic systems remain unknown. The neurohypophysial hormone oxytocin (OT) may offer an answer to this long-standing question because it is involved both in prosocial behavior and in the regulation of stress responses in mammals. In animals, OT has been implicated in a range of socially related behaviors, from sexual receptivity and grooming to territorial and protective maternal aggression. In humans, OT appears to have similarly variable effects, ranging from social receptiveness to suspiciousness and envy (5). After being synthesized in the magnocellular neurons of the paraventricular nucleus (PVN) and supraoptic nuclei OT is transported to the posterior lobe of the pituitary gland for storage and release. In addition to its peripheral actions, OT acts as a neurotransmitter in regions integrally involved in the stress response, especially the amygdala, hippocampus, and hypothalamus, via projections from the PVN (5–7). Accumulating evidence indicates that OT is involved in modulating stress responses, and its potential beneficial effects in secondary prevention—and possibly treatment—of PTSD have been investigated (5). However, the exact neurobiological mechanisms mediating effects of positive social contact and social interactions on stress-responsive physiologic systems are unknown. The study by Smith and Wang (8) in this issue of Biological Psychiatry offers exciting new evidence that points to OT levels in the PVN in mediating the effects of social support on the