Central kisspeptin injection enhances food consumption in broiler chickens: role of opioidergic and dopaminergic receptors

Kisspeptin, acting as both a neuropeptide and a hormone, known for its pivotal role in reproductive function and energy homeostasis, exerts multifaceted effects on central nervous system pathways involved in appetite regulation. Therefore, this study aimed to examine the impact of intracerebroventricular (ICV) infusion of kisspeptin on feeding behavior in neonatal broilers and to elucidate its interaction with the opioidergic and dopaminergic systems within the hypothalamic circuits governing appetite. Across seven separate experiments, broilers were systematically allocated into four different treatment groups for each experiment. In the initial experiment, neonatal chickens received ICV injections of saline or kisspeptin at escalating doses (0.25, 0.5, and 1 nmol). Subsequent experiments assessed the interplay between kisspeptin (1 nmol) and opioidergic modulators: β-FNA (mu opioid receptor antagonist), nor-BNI (kappa opioid receptor antagonist), and NTI (delta opioid receptor antagonist), as well as dopaminergic agents: l-DOPA (Dopamine precursor), SCH 23390 (D1 receptor antagonist), and AMI-193 (D2 receptor antagonist). Treatments included individual injections and simultaneous co-administrations of kisspeptin with these pharmacological agents. Feed consumption was quantitatively measured for 120 min post-infusion. Kisspeptin administration elicited a dose-dependent augmentation in feed consumption (P < 0.05). Co-infusion of l-DOPA+ kisspeptin inhibited the orexigenic effect induced by kisspeptin (P < 0.05). However, simultaneous infusion of β-FNA and SCH 23390 with kisspeptin markedly increased kisspeptin-stimulated hyperphagia (P < 0.05). The data indicate that kisspeptin promotes hyperphagia in neonatal broiler-type chickens, and the hyperphagic response is mediated through mu-opioid and D1-dopaminergic receptor pathways.