Feeding: Satiety Signal from Intestine Triggers Brain's Noradrenergic Mechanism

TLDR

Noradrenergic neurons in the hypothalamus that regulate feeding and satiety are activated by gastrointestinal receptors. The authors used localized push‑pull perfusion to characterize in vivo norepinephrine activity at medial and lateral hypothalamic sites. Injection of norepinephrine into the medial hypothalamus triggered spontaneous feeding, whereas lateral injection had no effect, and duodenal nutrient infusion increased norepinephrine release at lateral sites while suppressing it at medial sites, suggesting duodenal signals terminate feeding via hypothalamic noradrenergic inhibition.

Abstract

Noradrenergic neurons in the hypothalamus involved in feeding and satiety are activated by gastrointestinal receptors. In the unrestrained rat, sites were first identified at which norepinephrine injected in the medial hypothalamus caused spontaneous feeding, or in the lateral hypothalamus caused no response. The activity of in vivo norepinephrine at these two sites was characterized by localized push-pull perfusion. When a nutrient was infused directly into the rat's duodenum, the synaptic release of hypothalamic norepinephrine was enhanced at lateral sites insensitive to norepinephrine, but suppressed at medial sites reactive to norepinephrine. Thus, signals from duodenal receptors are conceivably sent to the rat's brain to end feeding by way of noradrenergic inhibitory neurons in the hypothalamus.