Abstract

Aim Dopaminergic, serotoninergic, and GABAergic systems influence feeding; however, it is unknown how these chemicals interact with neuromedin U (NMU)-induced feeding in birds. In the current study, ten trials were conducted to determine the links between the above-mentioned systems and NMU. Materials and Methods In the foremost experimentation, chickens were given intracerebroventricularly injections of NMU (0.1, 1, and 10 µg). NMU (10 µg), SCH23390 (5 nmol), a D1 receptor antagonist, and NMU + SCH23390 were administered in the second experiment. In subsequent experiments, instead of SCH23390, were applied AMI-193 (5 nmol D2 receptor antagonist), NGB2904 (6.4 nmol D3 receptor antagonist), L-741,742 (6 nmol D4 receptor antagonist), 6-OHDA (2.5 nmol dopamine inhibitor), SB242084 (5-HT2c receptor antagonist, 1.5 μg), 8-OH-DPAT (5-HT1A receptor agonist, 15.25 nmol), picrotoxin (GABAA receptor antagonist, 0.5 μg), and CGP54626 (GABAB receptor antagonist, 20 ng). Then, cumulative intake of food was recorded for 2 h. Results According to the results, NMU reduced feeding when compared to the control group (p < 0.05). The NMU-induced hypophagia was reduced with co-injection of NMU and SCH23390 (p < 0.05). Hypophagia was diminished with NMU and AMI-193 (p < 0.05). NMU + NGB2904 and NMU + L-741,742 co-injections had no influence (p > 0.05). 6-OHDA reduced the hypophagia (p < 0.05). NMU and SB242084 decreased the hypophagia (p < 0.05), whereas NMU and 8-OH-DPAT had no effect (p > 0.05). The effects were amplified with picrotoxin (p < 0.05). NMU with CGP54626 had no influence on the hypophagia (p > 0.05). Conclusion Thus, NMU-induced hypophagia is probably mediated by D1/D2, 5-HT2c, and GABAA receptors in neonatal chicks.

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