Abstract
Subregions within insular cortex and medial prefrontal cortex (mPFC) have been implicated in eating disorders; however, the way these brain regions interact to produce dysfunctional eating is poorly understood. The present study explored how two mPFC subregions, the infralimbic (IL) and prelimbic (PRL) cortices, regulate sucrose hyperphagia elicited specifically by a neurochemical manipulation of the agranular/dysgranular region of gustatory insula (AI/DI). Using intra-AI/DI infusion of the mu-opioid receptor (µ-OR) agonist, DAMGO (1 µg), sucrose hyperphagia was generated in ad-libitum-maintained rats, while in the same rat, either the IL or prelimbic (PRL) subregion of mPFC was inactivated bilaterally with muscimol (30 ng). Intra-IL muscimol markedly potentiated AI/DI DAMGO-induced sucrose hyperphagia by increasing eating bout duration and food consumption per bout. In contrast, PRL attenuated intra-AI/DI DAMGO-driven sucrose intake and feeding duration and eliminated the small DAMGO-induced increase in feeding bout initiation. Intra-IL or -PRL muscimol alone (i.e., without intra-AI/DI DAMGO) did not alter feeding behavior, but slightly reduced exploratory-like rearing in both mPFC subregions. These results reveal anatomical heterogeneity in mPFC regulation of the intense feeding-motivational state engendered by µ-OR signaling in the gustatory insula: IL significantly curtails consummatory activity, while PRL modestly contributes to feeding initiation. Results are discussed with regard to potential circuit-based mechanisms that may underlie the observed results.