Role of CRF system in a model of binge eating in female rats

Binge eating (BE) may be caused by a unique interaction between dieting and stress. Hence we considered interesting to evaluate the role of corticotrophin releasing factor 1 receptor (CRF-1R) mechanisms in BE. Four groups of female rats were used: NR+NS was normally fed and not stressed on the test day (d25); NR+S was fed as NR+NS and stressed on d25; R+NS was exposed to 3 cycles of yo-yo dieting but not stressed; R+S was fed as R+NS and stressed on d25. All groups were fed with highly palatable food (HPF) for 2 h on day 5-6 and 13-14. Stress was induced by preventing access to HPF for 15 min, while rats were able to see and smell it. After the stressful procedure the rats had free access to HPF and standard chow. BE was observed only in the R+S group and injections of R121919 (10-20 mg/kg, s.c.) significantly reduced it Endocrinological analysis revealed marked increase of CORT levels under R+S conditions. On the other hand, metyrapone (50 and 100 mg/kg), a CORT synthesis inhibitor, did not prevent BE, neither CORT injection (2.5 and 10 mg/kg) induced it. When CRHR1 gene expression was monitored, an up-regulation in the BNST, central (CeA) and basolateral amygdala (BLA) of R+S rats was found. Of note, bilaterally injection of the non selective CRF receptor antagonist D-Phe-CRF(12-41) (50 ng/rat) into the BNST potently and selectively reduced BE. Altogether these findings demonstrated that extra-hypothalamic CRF-1R related mechanisms rather than the endocrine function of these receptors are involved in BE.