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Physiology, Endocrinology & Reproduction

Serotonin-induced hypophagia is mediated via α2 and β2 adrenergic receptors in neonatal layer-type chickens

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Pages 298-304 | Received 20 Nov 2015, Accepted 27 Oct 2016, Published online: 31 Mar 2017
 

ABSTRACT

1. Serotoninergic and adrenergic systems play crucial roles in feed intake regulation in avians but there is no report on possible interactions among them. So, in this study, 5 experiments were designed to evaluate the interaction of central serotonergic and adrenergic systems on food intake regulation in 3 h food deprived (FD3) neonatal layer-type chickens.

2. In Experiment 1, chickens received intracerebroventricular (ICV) injection of control solution, serotonin (56.74 nmol), prazosin (α1 receptor antagonist, 10 nmol) and co-injection of serotonin plus prazosin. In Experiment 2, control solution, serotonin (56.74 nmol), yohimbine (α2 receptor antagonist, 13 nmol) and co-injection of serotonin plus yohimbine were used. In Experiment 3, the birds received control solution, serotonin (56.74 nmol), metoprolol (β1 receptor antagonist, 24 nmol) and co-injection of serotonin plus metoprolol. In Experiment 4, injections were control solution, serotonin (56.74 nmol), ICI 118.551 (β2 receptor antagonist, 5 nmol) and serotonin plus ICI 118.551. In Experiment 5, control solution, serotonin (56.74 nmol), SR59230R (β3 receptor antagonist, 20 nmol) and co-administration of serotonin and SR59230R were injected. In all experiments the cumulative food intake was measured until 120 min post injection.

3. The results showed that ICV injection of serotonin alone decreased food intake in chickens. A combined injection of serotonin plus ICI 118.551 significantly attenuated serotonin-induced hypophagia. Also, co-administration of serotonin and yohimbine significantly amplified the hypophagic effect of serotonin. However, prazosin, metoprolol and SR59230R had no effect on serotonin-induced hypophagia in chickens.

4. These results suggest that serotonin-induced feeding behaviour is probably mediated via α2 and β2 adrenergic receptors in neonatal layer-type chicken.

Acknowledgements

This research was supported by a grant from the Research Council of the Faculty of Veterinary Medicine, University of Tehran, Iran. This manuscript does not contain any studies with human subjects performed by any of the authors. All experiments were executed according to the Guide for the Care and Use of Laboratory Animals (NIH publication No. 85-23, revised 1996) and approved by the institutional animal ethics committee.

Disclosure statement

M. Zendehdel, F. Sardari, S. Hassanpour, M. Rahnema, A. Adeli and E. Ghashghayi declare that they have no conflict of interest.

Additional information

Funding

This work was supported by the Research Council of the Faculty of Veterinary Medicine, University of Tehran.

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