Feeding: satiety signal from intestine triggers brain's noradrenergic mechanism.

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.