NPY1 and MC3/MC4 receptors mediate BDNF-induced hypophagia in 5-day-old chickens

Distinguishing the variables that control craving and examining the interaction between them can improve the efficiency of livestock breeding, genetic modification, and drug treatments of obesity-related complications. Hence, in the current study, we investigated the interaction between neuropeptide Y and melanocortinergic systems with brain-derived neurotrophic factor (BDNF) in regulating broilers' feed intake. The present study was conducted on 264 broiler chickens in 6 experiments. In experiment 1, chickens received intracerebroventricular (ICV) infusion of BDNF (7.5, 15, and 30 μg) after 3 h of food deprivation. BIBP-3226 (NPY1 receptor antagonist, 1.25 nmol), BDNF (30 μg), and BDNF + BIBP-3226 were administrated in the second treatment. Experiments 3-6 were similar to treatment 2, except birds were infused with BIIE 0246 (NPY2 receptor antagonist, 1.25 nmol), CGP71683A (NPY5 receptor antagonist, 1.25 nmol), SHU9119 (MC3/MC4 receptor antagonist, 0.5 nmol) and MCL0020 (MC4 receptor antagonist, 0.5 nmol) instead of BIBP-3226. Then, cumulative meal intake was recorded for 2 hours. Based on observations, BDNF injection (15 and 30 μg) caused significant hypophagia at all test times (p<0.05). The co-infusion of NPY2 and NPY5 receptor antagonists with BDNF did not affect BDNF-induced hypophagia (p>0.05), while the infusion of NPY1 receptor antagonist + BDNF caused a significant strengthening of this effect (p<0.05). Also, despite the lack of significant effect of MC4 receptor antagonist + BDNF administration on the appetite-reducing effect of BDNF (p>0.05), simultaneous infusion of MC3/MC4 receptor antagonist and BDNF suppressed hypophagia (p<0.05). Finally, it appears that MC3/MC4 and NPY1 receptors mediate BDNF-induced hypophagia in 5-day-old broiler chickens.