title: Hypothalamic oxytocin mediates social buffering of the stress response.
abstract: BACKGROUND
  While stressful life events can enhance the risk of mental disorders, positive social interactions can propagate good mental health and normal behavioral routines. Still, the neural systems that promote these benefits are undetermined. Oxytocin is a hormone involved in social behavior and stress; thus, we focus on the impact that social buffering has on the stress response and the governing effects of oxytocin.
  
  
  METHODS
  Female prairie voles (Microtus ochrogaster) were exposed to 1 hour immobilization stress and then recovered alone or with their male partner to characterize the effect of social contact on the behavioral, physiological, and neuroendocrine stress response. In addition, we treated immobilized female voles recovering alone with oxytocin or vehicle and female voles recovering with their male partner with a selective oxytocin receptor antagonist or vehicle. Group sizes varied from 6 to 8 voles (N = 98 total).
  
  
  RESULTS
  We found that 1 hour immobilization increased anxiety-like behaviors and circulating levels of corticosterone, a stress hormone, in female prairie voles recovering alone but not the female prairie voles recovering with their male partner. This social buffering by the male partner on biobehavioral responses to stress was accompanied by increased oxytocin release in the paraventricular nucleus of the hypothalamus. Intra-paraventricular nucleus oxytocin injections reduced behavioral and corticosterone responses to immobilization, whereas injections of an oxytocin receptor antagonist blocked the effects of the social buffering.
  
  
  CONCLUSIONS
  Together, our data demonstrate that paraventricular nucleus oxytocin mediates the social buffering effects on the stress response and thus may be a target for treatment of stress-related disorders.
authors.affiliation: Department of Psychology and Program in Neuroscience, Florida State University, Tallahassee, Florida. Electronic address: asmith@neuro.fsu.edu.
authors.forename: Adam S
authors.initials: AS
authors.lastname: Smith
authors.affiliation: Department of Psychology and Program in Neuroscience, Florida State University, Tallahassee, Florida.
authors.forename: Zuoxin
authors.initials: Z
authors.lastname: Wang
mesh_terms: D000818:Animals; D001007:Anxiety / Q000503:physiopathology; D003411:Arvicolinae; D003345:Corticosterone / Q000097:blood; D005260:Female; D009043:Motor Activity / Q000502:physiology; D010121:Oxytocin / Q000378:metabolism*; D010152:Pair Bond; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000503:physiopathology*; D011897:Random Allocation; D018045:Receptors, Oxytocin / Q000037:antagonists & inhibitors / Q000378:metabolism; D012149:Restraint, Physical; D012919:Social Behavior; D012934:Social Isolation; D013315:Stress, Psychological / Q000503:physiopathology*
chemical_list: D018045:Receptors, Oxytocin; D010121:Oxytocin; D003345:Corticosterone
keywords: Corticosterone; HPA axis; elevated plus maze; immobilization stress; pair-bond; social buffering