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 α1‐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 α2‐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 α2, but not α1 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 α2‐receptors. These results are consistent with the view that octopamine may function as a modulator of NA activity in the central nervous system.