Factors influencing feeding elicited by intracranial noradrenaline in rats

Modulation of sibutramine‐induced increases in extracellular noradrenaline concentration in rat frontal cortex and hypothalamus by α2‐adrenoceptors

“…Firstly, they are consistent with in vitro evidence that the active metabolites of this drug are potent inhibitors of noradrenaline uptake (Cheetham et al ., 1996). Nevertheless, the finding that sibutramine increases noradrenaline in the region of the PVN is at variance with a long‐standing hypothesis that increasing extracellular noradrenaline in this hypothalamic region markedly facilitates feeding behaviour (Matthews et al ., 1977; Leibowitz, 1978). This effect is thought to be mediated by noradrenergic activation of postsynaptic α 2 ‐adrenoceptors (Goldman et al ., 1985).…”

“…The first aim of this study was to establish the effects of sibutramine on extracellular noradrenaline concentration in the hypothalamus using in vivo microdialysis, and to compare these effects with those in the frontal cortex. Drug‐induced changes in extracellular noradrenaline concentration were monitored in the region of the paraventricular nucleus (PVN) because changes in noradrenergic activity in this specific area of the hypothalamus show the greatest influence on food intake compared with other brain regions (Matthews et al ., 1977; Leibowitz, 1978; Wellman, 1992). Increased noradrenergic activity in the hypothalamus has been associated with both an increase and decrease in feeding behaviour; activation of α 1 ‐adrenoceptors with phenylpropanolamine induces a suppression of food intake, whereas activation of α 2 ‐adrenoceptors with clonidine has a biphasic effect, with low doses facilitating and high doses inhibiting food intake (Wellman, 1992).…”

Time-dependent effects of intrahypothalamic injection of vasoactive intestinal peptide on spontaneous motor activity in rats.

“…When administered directly in the PV or VM during the light cycle, it induced feeding responses in satiated rats (LEIBOwITz, 1978;MATTHEWS et al, 1978), and when administered in the lateral hypothalamus, it inhibited feeding during the light cycle and facilitated during the dark cycle (MARGULES et al, 1972) in rats. Taking the finding into consideration that destruction of noradrenergic bundles with 6-hydroxydopamine facilitated feeding only in the dark cycle (AHLSKOG et al, 1975), it seems that the noradrenergic transmission exerts, as a whole, an influence on the hypothalamic nuclei to prevent overeating in the dark cycle, whereas it exerts some facilitatory influence in the light cycle.…”

Neurochemistry of appetite mechanisms

“…VMH lesions increase energy intake selectively over protein intake (Anderson, Leprohon & Coscina, 1978). Extra energy storage after VMH lesions would create a secondary desatiation of energy appetite, until accumulated fat provided a background satiety which reduced daily food intake (Booth, 1978).…”

“…Most 5-HT lies in the gut and varies with feeding (Biggio, Piccardi, Porceddu & Gessa, 1977). Fenfluramine slows gastric emptying (Page, Morville & Corkey, 1978), which can have metabolic and behavioural consequences (Booth, 1978) in addition to any primary metabolic action of the drug (Petrie, Mowat, Bewsher & Stowers, 1975).…”