Glucocorticoids have major effects on food intake, demonstrated by the decrease of food intake following adrenalectomy. Satiety signals are relayed to the nucleus of the solitary tract (NTS), which has reciprocal projections with arcuate (ARC) and paraventricular nucleus (PVN) of the hypothalamus. We evaluated the effects of glucocorticoids on the activation of hypothalamic and NTS neurons induced by food intake in rats subjected to adrenalectomy (ADX) or sham surgery seven days before the experiments. Half of ADX animals received corticosterone (ADX+B) in the drinking water (B: 25mg/l). Fos/tyrosine hydroxylase (TH), Fos/corticotrophin-releasing factor (CRF) and Fos immunoreactivity were assessed in the NTS, PVN and ARC, respectively. Food intake and body weight were reduced in the ADX group compared to sham and ADX+B groups. Fos and Fos/TH in the NTS, Fos and Fos/CRF immunoreactive neurons in the PVN and Fos in the ARC were increased after refeeding, with higher number in the ADX group, compared to sham and ADX+B groups. CCK administration showed no hypophagic effect on ADX group despite similar increase of Fos/TH immunoreactive neurons in the NTS, compared to sham and ADX+B, suggesting that CCK alone cannot further increase the anorexigenic effect induced by glucocorticoid deficiency. The present data indicate that glucocorticoid withdrawal reduced food intake, which was associated with higher activation of ARC, CRF neurons of the PVN and catecholaminergic neurons of the NTS. In the absence of glucocorticoids, satiety signals elicited during a meal lead to an augmented activation of brainstem and hypothalamic pathways.