Insulin-induced elevation of hypothalamic norepinephrine turnover persists after glucorestoration unless feeding occurs.

We employed a delayed feeding paradigm to assess regional brain catecholamine changes associated with insulin-elicited glucoprivic feeding. This paradigm makes use of the recent discovery that glucoprivic challenges significantly enhance food intake even when food is withheld until other signs of glucoprivation have abated. Using this paradigm we attempted to temporally dissociate the neurochemical events associated with the ingestive response from other potentially confounding consequences of insulin or glucoprivation. We found a high degree of congruence between elevated hypothalamic norepinephrine (NE) turnover (estimated by the change in transmitter concentration after synthesis inhibition) and the persistence of hunger, both during and after apparent glucoprivation. In the absence of food, hypothalamic NE turnover was enhanced during insulin-induced glucoprivation and this increase persisted into the postglucoprivic period. A brief feeding bout, either during glucoprivation or postglucoprivically, rapidly normalized NE turnover rates. Moreover, brief access (30 min) to a limited quantity of food (2.5 g) during glucoprivation abolished both the elevated turnover and the feeding response otherwise observed postglucoprivically. Turnover of catecholamines in the telencephalon was also enhanced after insulin, but the increased activity did not persist into the postglucoprivic period and, in addition, was not altered in any consistent manner by food intake. These findings strengthen the view that hypothalamic NE neurons are involved in the mediation of glucoprivic feeding.