Research articleThe central effects of alpha-melanocyte stimulating hormone (α-MSH) in chicks involve changes in gene expression of neuropeptide Y and other factors in distinct hypothalamic nuclei

- The hypothalamic mechanisms that mediate the effects of α-MSH on food intake in birds are unclear.
- Central α-MSH increased chick c-Fos immunoreactivity in the ARC, DMN, LH, and PVN.
- α-MSH increased NPY and AgRP mRNA in the ARC and reduced NPYR1 mRNA in the PVN.
- In the DMN, NPY and DDC mRNAs increased in α-MSH-treated chicks.
- Results suggest that α-MSH treatment affects NPY/AgRP production and signaling.

Alpha-melanocyte stimulating hormone (α-MSH) is a satiety-inducing factor in birds and mammals although central mechanisms mediating its effects on appetite in birds are poorly understood. Thus, the objective of the present study was to determine effects of centrally-injected α-MSH on c-Fos and gene expression in chick appetite-associated hypothalamic nuclei. At 4 days post-hatch, 3 h-fasted chicks were intracerebroventricularly (ICV) injected with 0 (vehicle) or 0.12 nmol α-MSH and 1 h later, hypothalamus samples were collected for measuring c-Fos immunoreactivity and mRNA abundance of appetite-associated factors in hypothalamic nuclei. There were more c-Fos immunoreactive cells in the arcuate nucleus (ARC), dorsomedial nucleus (DMN), lateral hypothalamus (LH), and paraventricular nucleus (PVN) of α-MSH- than vehicle-injected chicks. Neuropeptide Y (NPY), oxytocin receptor (OXTR), and agouti-related peptide (AgRP) mRNAs were greater in α-MSH- than vehicle-injected chicks in the ARC. In the PVN, NPY receptor sub-type 1 (NPYR1) mRNA was reduced while c-Fos mRNA was increased in response to treatment with α-MSH. NPY, c-Fos, and DOPA decarboxylase (DDC) mRNAs were greater in treated than vehicle-injected chicks in the DMN. Results suggest that during the first hour post-injection, the appetite-inhibiting effects of α-MSH involve activation of the ARC, DMN, PVN, and LH, and corresponding changes in transcriptional regulation of factors involved with NPY, AgRP and mesotocin signaling, and monoamine synthesis. The effects of these changes may include an inhibition of NPY signaling in the PVN to induce satiety and stimulation of NPY/AgRP neurons in the ARC in an attempt to restore homeostatic levels of food intake.