Functional interaction between nociceptin/orphanin FQ and α-melanocyte-stimulating hormone in the regulation of feeding

• Published in: Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2006-07, Vol.27 (7), p.1827-1834
• Main Authors: Bomberg, Eric M., Grace, Martha K., Levine, Allen S., Olszewski, Pawel K.
• Format: Article
• Language: English
• Subjects: alpha-MSH - physiology; Animals; Biological and medical sciences; c-Fos; Cerebral Ventricles - metabolism; Eating; Feeding; Feeding Behavior; Food Deprivation; Fundamental and applied biological sciences. Psychology; Injection; Male; Melanocortins; Neurons - metabolism; Nociceptin; Opioid Peptides - physiology; Orphanin FQ; Proto-Oncogene Proteins c-fos - metabolism; Rats; Rats, Sprague-Dawley; Vertebrates: endocrinology; α-Melanocyte-stimulating hormone
• ISSN: 0196-9781; 1873-5169
• DOI: 10.1016/j.peptides.2006.02.007

Nociceptin/orphanin FQ (N/OFQ), an endogenous agonist of the opioid N/OFQ (NOP) receptor, increases food intake when administered centrally. As N/OFQ is part of a larger neural network that governs consummatory behavior, presumably its orexigenic properties stem from interplay with other neuropeptidergic components of the feeding-related circuitry. One such peptide may be the ligand of the melanocortin-3 and -4 receptors, α-melanocyte-stimulating hormone (α-MSH), which is known to inhibit food intake. The aim of the present study was to establish whether there is a functional “interaction” between N/OFQ and α-MSH in the regulation of feeding. By using double immunostaining for c-Fos and α-MSH, we found that intracerebroventricular (i.c.v.) injection of N/OFQ at a 10 nmol dose that moderately prolongs deprivation-induced food intake in rats, decreases activation of α-MSH neurons involved in feeding termination. However, i.c.v. injections of α-MSH at doses previously established to reduce deprivation-induced feeding, do not decrease hyperphagia generated by N/OFQ in ad libitum-fed animals. Our results suggest that while α-MSH does not appear to modify the orexigenic response to N/OFQ in sated rats, the NOP receptor ligand promotes a decrease in activation of neurons synthesizing the anorexigenic peptide, α-MSH, at the time of re-feeding. Thus, to some degree, the stimulatory effect of N/OFQ on consumption may arise from this peptide's inhibitory influence on activity of anorexigenic pathways containing α-MSH.