Social defeat stress activates medial amygdala cells that express type 2 corticotropin-releasing factor receptor mRNA
Abstract Defeat is a social stressor involving subordination by a threatening conspecific. Type 2 corticotropin-releasing factor receptors (CRF2 ) are abundant in brain regions implicated in defeat responses and are putative stress-related molecules. The present study sought to determine whether neu...
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Veröffentlicht in: | Neuroscience 2009-08, Vol.162 (1), p.5-13 |
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Sprache: | eng |
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Zusammenfassung: | Abstract Defeat is a social stressor involving subordination by a threatening conspecific. Type 2 corticotropin-releasing factor receptors (CRF2 ) are abundant in brain regions implicated in defeat responses and are putative stress-related molecules. The present study sought to determine whether neuroactivation and CRF2 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 CRF2 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 CRF2 mRNA and Fos-positive cells was observed in the posterior medial amygdala but not in the arcuate nucleus or ventromedial hypothalamus. The results indicate CRF2 receptor-positive neurons in the posterior medial amygdala are involved in the neural response to social defeat. |
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ISSN: | 0306-4522 1873-7544 |
DOI: | 10.1016/j.neuroscience.2009.03.078 |