Glucocorticoids released by stress bind to glucocorticoid(GR) and/or mineralocorticoid receptors(MR) to exert negative feedback of subsequent hypothalamic-pituitary-adrenal(HPA) responses to stress. Feedback inhibition is implicated in habituation of HPA activity to repeated exposure to the same(homotypic) stressor. We hypothesized that the posterior paraventricular thalamus(pPVTh) is a site where corticosterone acts to exert negative feedback during repeated stress which is important for habituation. As previously reported, the pPVTh inhibits HPA responses to homotypic and heterotypic stressors in repeatedly, but not acutely, stressed rats. We conducted a series of experiments involving intra-pPVTh administration of MR and/or GR agonists or antagonists during different time frames over 8 days of restraint. MRs exist in the pPVTh, as do GRs as shown by our immunocytochemical results. Acute intra-pPVTh injection of MR and/or GR antagonist before the 8th restraint did not alter expression of habituation. Since habituation may develop before day 8, we manipulated GRs+MRs in the pPVTh throughout 8 days of stress using intra-pPVTh corticosterone implants, which enhanced habituation on day 8 without affecting acute stress responses. Conversely, daily intra-pPVTh injections of GR+MR antagonists on days 1-7 of restraint prevented habituation on day 8. These data suggest that corticosterone released during repeated stress can act at GRs+MRs in the pPVTh to inhibit HPA responses to homotypic stress. We also found that some GR-containing cells in the pPVTh project to the medial prefrontal cortex and basolateral amygdala, suggesting that pPVTh-induced inhibition of HPA activity is potentially mediated by its projections to these select limbic structures.