Ingestive behavior after intracerebral and intracerebroventricular infusions of glucose and 2-deoxy-D-glucose

Abstract

Direct infusions of 2-DG into the lateral hypothalamic area (LHA), the ventromedial hypothalamus (VMH), the dorsal hippocampus, the amygdaloid complex or the caudate nucleus were all ineffective in eliciting drinking or feeding in satiated rats. However, 2-DG (but not D-glucose) infused into the lateral ventricles of satiated rats elicited feeding preceded by an initial burst of drinking, which could be blocked by prior intraventricular infusion of the alpha-adrenergic antagonist, phentolamine, by the serotonergic blocker, methysergide, but only slightly by the dopaminergic receptor blocker, spiroperidol. The feeding response was totally blocked by phentolamine but not by methysergide or spiroperidol. These results show that 1) intraventricular administration of 2-DG can induce feeding, as well as drinking, supporting the hypothesis of cerebral glucoreceptors for the initiation of feeding behavior; and 2) local cytoglucopenia in the LHA, the VMH, or other limbic structures is not sufficient to initiate feeding. It is hypothesized that a specific pattern of cerebral glucoprivation rather than local glucoprivation, or an action of 2-DG on the presynaptic membrane of noradrenergic "feeding neurons" could be the mechanisms of 2-DG-induced feeding.