Satiety induced by neuropeptide FF and gastrin in birds

Mammalian and avian species differ in some appetite-related aspects including how and which neurotransmitters and hormones regulate appetite. The objective of this research was to determine how two satiety-inducing neuropeptides regulate feeding behavior in avian models. Neuropeptide FF (NPFF) was intracerebroventricularly (ICV) injected into Japanese quail and decreased food intake at a dose of 32 nmol. NPFF-injected quail had increased expression levels of hypothalamic melanocortin subtype 3 receptor and decreased expression levels of neuropeptide Y receptor subtype 1 mRNAs compared to vehicle-injected controls. In a second study, gastrin was ICV injected into broiler chicks and decreased food intake at a dose of 500 ng (0.12 nmol). There was increased c-Fos immunoreactivity in the lateral hypothalamus (LH), paraventricular nucleus (PVN), arcuate nucleus, nucleus of the solitary tract, and area postrema at 1 h post-injection. Although a variety of genes were measured in those activated nuclei, there were only differences in melanin-concentrating hormone mRNA in the LH and corticotropin-releasing factor (CRF) mRNA in the PVN, suggesting that CRF signaling was involved in the hypothalamic response to gastrin. However, co-injection of gastrin and astressin, a CRF receptor antagonist did not affect gastrin-induced suppression of food intake, implying that the CRF receptors may not be directly associated with gastrin-induced satiety. Identifying the molecular pathways that mediate the effects of anorexigenic neuropeptides in birds will lead to the development of novel treatment options for appetite-related diseases and increased understanding of factors that affect production efficiency in commercial poultry and survival/resource allocation in wild birds.