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Analysis of stress-induced CRH, CRHR1, AVP and mineralocorticoid receptor (MR) mRNA expression in C57/Bl6 mice: Implications for HPA-system regulation
The importance of maintaining stress-induced HPA system activation within tolerable limits requires efficient mechanisms for feedback inhibition. Lack of control and persistent uncertainty in prolonged stressful situations can result in chronically elevated levels of circulating corticosteroid hormones, what is believed to enhance vulnerability to a variety of diseases. Although detailed analyses of HPA-system modulation have been performed in rats, very little is known about central HPA feedback mechanisms in mice. Both hypothalamic CRHR1 and hippocampal MR have been suggested to be involved in central feedback mechanisms of HPA system regulation.
To further elucidate these neuroendocrine pathways, 24 male C57/Bl6 mice were killed under basal conditions or 2, 4, 12 and 24h following 30 minutes of restraint stress. In situ hybridization for CRH, CRHR1, AVP and MR mRNA with semiquantitative expression analysis was performed. Detailed analyses of the time-course of basal and stress-induced changes in mRNA expression in brain areas involved in the stress response (PVN, hippocampus, amygdala, neocortex) will be discussed with respect to potential implications for HPA-system regulation.