20 - Psychopharmacology of norepinephrine in eating disorders

Summary

Basic research on norepinephrine and feeding

One of the first studies investigating the relationship of the noradrenergic system to feeding behavior was conducted by Ritter et al. In this study the authors found that intraventricular injections of the α-adrenergic receptor agonist clonidine caused rats to eat voraciously; however, the injection of L-norepinephrine (L-NE) facilitated feeding but was not nearly as potent. The authors concluded that the relationship of noradrenergic mechanisms to feeding appeared to be a respondent one in which feeding was sensitized or disinhibited by activation of α-adrenergic receptors rather than an operant regulation that would be reinforced by the release of NE. Using a brain-cannula technique Leibowitz found that injection of NE into the paraventricular nucleus (PVN) elicited feeding in satiated rats and enhanced feeding in already hungry rats. Using midbrain lesions, fluorescence histochemistry, and brain cannulation, Leibowitz and Brown showed that the dorsal component of the central tegmental track contains the crucial noradrenergic axons that innervate the PVN and mediate noradrenergic stimulation of feeding behavior. They also determined that a strong reduction of loss of the feeding response was elicited by PVN injection of the presynaptic-acting drugs tranylcypromine and desipramine as well as showing a potentiation of the feeding response produced by injected NE. Russek et al. found that intraperitoneal injections of NE produced a marked decrease in feeding in several different feeding conditions. The authors postulated that NE was stimulating hepatic adrenergic receptors.