Stress-induced suppression of neuropeptide Y-induced hunger in anorexic chicks involves corticotropin-releasing factor signaling and the paraventricular nucleus of the hypothalamus

Abstract

The Virginia lines of chickens have been selected for low (LWS) or high (HWS) juvenile body weight and have different severities of anorexia and obesity, respectively. The LWS that are exposed to stressors at hatch are refractory to neuropeptide Y (NPY)-induced food intake and the objective was to elucidate the underlying mechanisms. Chicks were exposed to a stressor (-20°C for 6 minutes, and 22°C and delayed access to food for 24 hours) after hatch and hypothalamic nuclei, including the lateral hypothalamus (LH), paraventricular nucleus (PVN), ventromedial hypothalamus (VMH), and arcuate nucleus (ARC), were collected 5 days later. In LWS but not HWS, stress exposure up-regulated corticotropin-releasing factor (CRF), CRF receptor sub-types 1 and 2 (CRFR1 and CRFR2, respectively), melanocortin receptor 4, and urocortin 3 in the PVN, and CRFR2 mRNA in the VMH and ARC. In LWS, stress exposure was also associated with greater NPY and NPY receptor sub-type 5 mRNA in the ARC and PVN, respectively, and decreased AgRP mRNA in the ARC. In HWS, stress exposure was associated with increased CRFR1 and decreased CART in the ARC and PVN, respectively. Refractoriness of the food intake response to NPY in LWS may thus result from overriding anorexigenic tone in the PVN associated with CRF signaling. Indeed, the orexigenic effect of NPY was restored when LWS were injected with a CRF receptor antagonist, astressin, before stress exposure. These results provide insights into the molecular basis of eating disorders and suggest that CRF signaling in the PVN may exacerbate the anorexic phenotype in the presence of environmental stressors.

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