m ‐Octopamine injected into the paraventricular nucleus induces eating in rats: a comparison with noradrenaline‐induced eating

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 α 1 ‐adrenoceptor antagonist, corynanthine, and the β‐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 α 2 ‐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 α 2 , but not α 1 or β‐adrenoceptors. 4 Injection of α‐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 α 2 ‐receptors. These results are consistent with the view that octopamine may function as a modulator of NA activity in the central nervous system.