DESCRIPTION (provided by candidate): Traumatic events and chronic stress have been implicated in the development of stress-related psychopathologies such as post-traumatic stress disorder, depression, and anxiety disorders. Most animal models of stress-related disorders use tightly controlled, but artificial, stressors and it is critical to extend these findings to more biologically relevant stressors. In male Syrian hamsters, a single social defeat produces a prolonged reduction in territorial aggression and a concomitant rise in submissive and defensive behavior. We call this stress-induced change in agonistic behavior conditioned defeat. The overall hypothesis of the current proposal is that corticotrophin-releasing hormone (CRH) modulates the acquisition and expression of conditioned defeat by its actions on serotonin (5-HT) cells and 5-HT1a autoreceptors in the dorsal raphe nucleus (DRN). Specific Aim 1 will test the hypothesis that CRH neurotransmission within the DRN modulates the acquisition and expression of conditioned defeat. Specific Aim 2 will test the hypothesis that activation of 5-HT1a autoreceptors within the DRN modulates the acquisition and expression of conditioned defeat. Furthermore, Specific Aim 2 will test the hypotheses that social defeat activates 5-HT neurons and desensitizes 5-HT1a autoreceptors in the DRN. The experiments in the current proposal will provide valuable information on the neurobiological mechanisms underlying stress-related disorders.