Raclopride

Binge eating is a key feeding behavior that is a core symptom of most major eating disorders, with disruptions in the neurotransmitter dopamine gaining significant interest as a potential risk factor. In the current study we sought to examine functional and molecular changes that may underlie alterations in the dopamine system in female rats prone to binge eating. Rats received six feeding tests with intermittent access to palatable food (PF), which was used to identify binge eating resistant (BER) and prone (BEP) phenotypes based on examining tertiles across the feeding tests. Subsequently, rats received separate additional feeding tests following administration of either: the D1R agonist SKF 38393 (1.0, 3 mg/kg); D1R antagonist SCH 23390 (0.1, 0.3 mg/kg); D2/3R agonist quinpirole (0.03, 0.1 mg/kg); or the D2R antagonist, raclopride (0,1, 0.2 mg/kg). Stimulation of D1R reduced both PF and chow intake in BEP but not BER rats. Similarly, inhibition of D1R disrupted intake selectively in BEP rats, however these effects were restricted to PF intake. Alternatively, D2/3R stimulation inhibited PF intake in both groups of rats, although the suppression of PF intake was more prolonged in BEP rats. Blockade of D2Rs failed to impact feeding behavior in either group of rats. This general pattern of heightened responsivity to D1R manipulation was consistent with qPCR findings, which revealed in BEP compared to BER rats, a downregulation in the ventral tegmental area, and an upregulation in nucleus accumbens of D1R gene expression. Collectively these findings show that BEP rats overeat PF, which may be due to altered mesolimbic expression of D1R and corresponding heightened sensitivity to the rewarding properties of PF.