Neuroeconomics of Social Behavior Following Trauma Exposure

Impaired social functioning is a frequent and disabling sequela of trauma-related disorders. PTSD is associated with a high rate of severe impairment in quality of life relative to other anxiety disorders, including panic disorder, social phobia, and OCD, with particularly marked impairment in social quality of life. Mounting evidence indicates that impairment in quality of life in PTSD is strongly related to its effect on social functioning. Such difficulties are widespread and affect multiple social networks, including marital relationships, and friendships and family relationships. Social withdrawal, defined here in terms of reduced social network size, is of particular interest because of its strong relationship with health outcomes, including increased risk of disability, reduced immune response, and increased mortality risk; most critically, poor social integration is associated with a threefold increase in suicide risk. Because women are at a 2.3-to-3-fold increased risk compared to men of developing PTSD following trauma, understanding the differential neurobiological pathways that may contribute to the development of stress-related disorders in women is particularly critical. Women are more likely than men to endorse social detachment following trauma, especially when the trauma involves exposure to violence. In this project, we propose abnormal reward processing (anhedonia) as a specific mechanism underlying social withdrawal in trauma-exposed women, and we present a paradigm that capitalizes on advances in neuroeconomics to elucidate the neural underpinnings of social withdrawal. Additionally, we propose to identify the possible influences of a stress peptide (pituitary adenylate cyclase-activating polypeptide: PACAP) implicated in sex-specific changes in social behavior following stress exposure.