1 The effects on food intake in rats of injection of m-and p-octopamine into the paraventricular nucleus (PVN) of the hypothalamus were examined, and compared to the effects of noradrenaline (NA). 2 m-Octopamine injected into the PVN induced a dose-dependent increase in food intake, with the maximal effect occurring at a dose of 25 nmol. p-Octopamine did not elicit eating unless it was administered to animals pretreated with the monoamine oxidase inhibitor, pargyline. 3 The effects of pretreatment with various adrenoceptor antagonists, injected into the PVN, on the eating responses induced by 25 nmol m-octopamine and NA were examined. The a,1-adrenoceptor antagonist, corynanthine, and the fi-adrenoceptor antagonist, propranolol, failed to alter the eating induced by m-octopamine or NA. The effects of these two amines were susceptible to blockade of a2-adrenoceptors. Idazoxan reversed the eating induced by m-octopamine and noradrenaline. However, yohimbine was effective only against the eating induced by m-octopamine. Thus, both m-octopamine and NA appear to act via c2, but not a, or fi-adrenoceptors. 4 Injection of a-methyl-p-tyrosine into the PVN attenuated the effect of m-octopamine, but not of NA. This result suggests that m-octopamine elicits eating, at least in part, by releasing endogenous NA. 5 The NA and octopamine uptake inhibitor, desipramine, significantly potentiated the eating induced by a low dose of m-octopamine. This effect may occur because desipramine would prolong the synaptic activity of released NA. 6 The results indicate that m-octopamine elicits a marked and reliable eating response which is mediated largely by a release of endogenous NA, which acts at a2-receptors. These results are consistent with the view that octopamine may function as a modulator of NA activity in the central nervous system.