Rapid effects of glucocorticoids on adrenocorticotropin hormone (ACTH) secretion were first demonstrated by Dallman and Jones. Glucocorticoid fast feedback is believed to be dependent upon brain feedback sites, particularly the hippocampus. The current studies are part of a series of studies examining the links between hippocampal adrenal steroid receptor changes and changes in fast feedback. Our previous studies have demonstrated that chronic stress and chronic corticosterone injections are capable of diminishing the fast feedback effect of injected glucocorticoids on ACTH secretion. The current studies explore whether administration of a different form of exogenous corticosterone, a 50% corticosterone pellet, a treatment that leads to constant corticosterone levels of 7-8 micrograms/dl, was capable of affecting fast feedback. Rats were studied both before and after the implantation of the 50% corticosterone pellets. Administration of cortisol at the initiation of restraint stress resulted in decreased ACTH release over the course of 30 min in both the morning and afternoon before implantation of corticosterone pellets. Following the implantation of 50% corticosterone pellets, the overall ACTH stress response was diminished in both the morning and the afternoon. However, cortisol injection at the initiation of restraint stress continued to exert fast feedback effects on ACTH secretion. These studies suggest that constant low plasma corticosterone concentrations of 6-7 micrograms/dl are able to inhibit the overall stress response but not the ability to respond to fast feedback. This contrasts with our previous studies with a corticosterone injection paradigm which produced abnormalities in glucocorticoid fast feedback.