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

Abstract

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.

Involvement of brain ketone bodies and the noradrenergic pathway in diabetic hyperphagia in rats

“…Values are means ± SEM hypothalamic PVN potently elicits food intake in rats, and the PVN NE synthesis rate increases in 24-h fasting mice [37,38]. NE stimulates feeding via the a2-adrenergic receptor in the PVN in rats [42]. PVN NE-induced feeding is dependent on circulating corticosterone, and the PVN a2-adrenergic receptor is up-regulated by corticosterone in rats [43,44].…”

Inhibitory Effect of Octopamine on the Release of Endogenous Acetylcholine From Isolated Myenteric Synaptosomes of Guinea‐pig

“…Thus, the effect of octopamine on presynaptic a2adrenoceptors in cholinergic nerve terminals of guineapig ileum may be responsible for the inhibition of ACh release in the present study. The involvement of the release of endogenous noradrenaline by octopamine (Fletcher & Paterson 1989) to activate a2-adrenoceptors was ruled out by treatment with guanethidine (Starke 1972) and nomifensine (Iversen 1974). This result is consistent with the previous finding that dopamine inhibits ACh release through a-adrenoceptors using reserpinization and treatment with nomifensine (Gorich et al 1982).…”