Effects of corticosterone on corticotrophin-releasing hormone and gastrin-releasing peptide release in response to an aversive stimulus in two regions of the forebrain (central nucleus of the amygdala and prefrontal cortex)
Previous research has shown that chronic corticosterone treatment increases the expression of corticotrophin-releasing hormone (CRH) mRNA at the central nucleus of the amygdala (CeA). Like CRH, gastrin-releasing peptide (GRP) appears to be involved in mediation of the stress response and is released at the CeA during exposure to an acute stressor. Using in-vivo microdialysis, this study examined the effects of corticosterone treatment on the release of CRH and GRP in response to an airpuff challenge at two forebrain regions, the CeA and medial prefrontal cortex. Adrenally intact rats were treated with corticosterone by systemic implants over a 14-day period prior to microdialysis probe insertion. We found that, at both regions, the airpuff-induced CRH and GRP release were enhanced in the corticosterone pellet-implanted rats as compared with the release observed in the vehicle-implanted control rats. These findings suggest that chronic corticosterone exposure potentiates the stressor-elicited release of CRH and GRP. As cortisol dysregulation has frequently been reported in people with psychiatric conditions, such as anxiety disorders or depression, a better understanding of the glucocorticoid-mediating regulation of CRH and GRP may provide insight into the underlying neurochemical mechanisms involved in both adaptive fear-type responses and maladaptive responses leading to pathology.
|Keywords||Bombesin, Glucocorticoids, Microdialysis, Rat|
|Journal||European Journal of Neuroscience|
Merali, Z. (Zul), Anisman, H, James, J.S. (Jonathan S.), Kent, P. (Pam), & Schulkin, J. (Jay). (2008). Effects of corticosterone on corticotrophin-releasing hormone and gastrin-releasing peptide release in response to an aversive stimulus in two regions of the forebrain (central nucleus of the amygdala and prefrontal cortex). European Journal of Neuroscience, 28(1), 165–172. doi:10.1111/j.1460-9568.2008.06281.x