Corticotropin-releasing factor (CRF), but not corticosterone, increases basolateral amygdala CRF-binding protein.

Corticotropin-releasing factor (CRF) is a key mediator of the behavioral, autonomic, and endocrine responses to stress. CRF binds two receptors and a CRF-binding protein (CRF-BP), which may inactivate or modulate the actions of CRF at its receptors. The amygdala is an important anatomical substrate for CRF and contains CRF, its receptors, and CRF-BP. Our previous studies demonstrated that acute stress increases basolateral amygdala (BLA) CRF-BP mRNA. However, factors that may be responsible for this increase remain unclear. Both CRF and corticosterone are released during stress and are known to increase CRF-BP in vitro. However, the effects of these agents in vivo on brain CRF-BP have not been studied. Therefore, we examined the effects of CRF and corticosterone administration on BLA CRF-BP mRNA in rats. The findings demonstrate that intracerebroventricular CRF (5 microg) significantly increases BLA CRF-BP mRNA 9 h post-infusion, a time point consistent with that observed for the effects of acute stress-induced increases in CRF-BP. In contrast, injection of corticosterone at a dose mimicking acute stress (6.5 mg/kg sc) failed to increase BLA CRF-BP mRNA 9 h post-injection. Surprisingly, two different CRF antagonists failed to block CRF-induced increases in CRF-BP mRNA. These results suggest that CRF, but not corticosterone, may be responsible for stress-induced increases in BLA CRF-BP gene expression. Furthermore, this effect appears to be mediated by mechanisms other than the identified CRF receptors.