The interaction between ghrelin and bombesin or amylin administered intraperitoneally (ip) on food intake and brain neuronal activity was assessed by Fos-like immunoreactivity (FLI) in non-fasted rats. Ghrelin (13 µg/kg, ip) increased food intake compared to the vehicle group when measured at 30 min (g/kg: 3.66±0.80 vs. 1.68±0.42, p< 0.0087). Bombesin (8 µg/kg) injected ip with ghrelin (13 µg/kg) blocked the orexigenic effect of ghrelin (1.18±0.41 g/kg, p<0.0002). Bombesin alone (4 and 8 µg/kg, ip) exerted a dose-related non-significant reduction of food intake (g/kg: 1.08±0.44, p>0.45 and 0.55±0.34, p>0.16 respectively). By contrast, ghrelin-induced stimulation of food intake (g/kg: 3.96± 0.56 g/kg vs. vehicle 0.82±0.59, p<0.004) was not altered by amylin (1 and 5 µg/kg, ip) (g/kg: 4.37± 1.12, p>0.69, and 3.01±0.78, respectively, p>0.37). Ghrelin increased the number of FLI positive neurons/section in the arcuate nucleus (ARC) compared to vehicle (median: 42 vs. 19, p<0.008). Bombesin alone (4 and 8 µg/kg ip) did not induce FLI neurons in the paraventricular nucleus of the hypothalamus (PVN) and co-administered with ghrelin did not alter ghrelin-induced FLI in the ARC. However, bombesin (8 µg/kg) with ghrelin significantly increased neuronal activity in the PVN ~ 3-fold compared to vehicle and ~ 1.5-fold compared to the ghrelin group. Bombesin (8 µg/kg) with ghrelin injected ip induced Fos expression in 22.4±0.8 % of CRF-immunoreactive neurons in the PVN. These results suggest that peripheral bombesin, unlike amylin, inhibits peripheral ghrelin induced food intake and enhances activation of CRF neurons in the PVN.