• E M Fekete, Y Zhao, C Li, V Sabino, W W Vale, and E P Zorrilla.
• Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
• Neuroscience. 2009 Aug 4;162(1):5-13.

AbstractDefeat is a social stressor involving subordination by a threatening conspecific. Type 2 corticotropin-releasing factor receptors (CRF(2)) are abundant in brain regions implicated in defeat responses and are putative stress-related molecules. The present study sought to determine whether neuroactivation and CRF(2) expression co-occurred at brain region or cellular levels following acute defeat. Male "intruder" Wistar rats were placed into the cage of an aggressive "resident" Long-Evans rat (n=6). Upon defeat, intruders (n=6) were placed in a wire-mesh chamber and were returned to the resident's cage for an additional 75 min. Controls (n=6) were handled and returned to their home cage for the same duration. Coronal brain sections were stained for an immediate early gene product, Fos, as a neuronal activation marker. Combined immunohistochemistry with in situ hybridization was performed on a subset of brain sections from defeated intruders to visualize Fos immunoreactivity and CRF(2) mRNA jointly. Defeated rats had fivefold, sevenfold, and 10-fold more Fos-positive cells than controls in the arcuate, ventromedial nucleus of the hypothalamus, and medial amygdala post-defeat. Significant colocalization of CRF(2) mRNA and Fos-positive cells was observed in the posterior medial amygdala but not in the arcuate nucleus or ventromedial hypothalamus. The results indicate CRF(2) receptor-positive neurons in the posterior medial amygdala are involved in the neural response to social defeat.

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