Hypothalamic Hyperphagia: Dissociation from Hyperphagia Following Destruction of Noradrenergic Neurons

The results argue against recent suggestions that destruction of the ventral noradrenergic bundle mediates the classical hyperphagia syndrome associated with localized ventromedial hypothalamic lesions, and it is found that rats with MI unlike normal animals, tend not to a day-night variation in their foc.

Abstract

Major differences were found between classical hypothalamic hyperphagia in rats and the recently discovered hyperphagia syndrome resulting from destruction of the ventral noradrenergic bundle. Traditional medial hypothalamic lesions produced no detectable loss of norepinephrine, and the rats overate both in the daytime and at night, whereas destruction of the noradrenergic bundles with 6-hydroxydopamine depleted norepinephrine to 6 percent of normal and caused overeating only at night. Moreover, the two procedures were additive, not substitutive, in their effects on eating. These results argue against recent suggestions that destruction of the ventral noradrenergic bundle mediates the classical hyperphagia syndrome associated with localized ventromedial hypothalamic lesions. However, damage to noradrenergic pathways may contribute to the hyperphagia after extensive hypothalamic lesions.