Effects of Central Administration of Opioid Peptides, Vasotocin, Mesotocin, and Corticotrophin-Releasing Factor on Water Intake in Chicks

Abstract

Freedom from thirst is an undeniable requirement of the poultry industry. However, the regulatory mechanisms underlying water intake in chicks are not yet fully understood. In humans, increased blood osmolality is probably the strongest signal for drinking. Angiotensin II, a hyperosmotic signal, induces water intake in chickens; this effect is attenuated by an opioid receptor antagonist. Vasotocin and mesotocin appear to have osmoregulatory functions in chicken. Dehydration activates brain corticotrophin-releasing factor (CRF) neurons in rats, and the central administration of CRF induces water intake in rabbits. This study aimed to clarify the effects of neuropeptides such as opioid peptides, vasotocin, mesotocin, and CRF on water intake to identify thirst-inducing neuropeptides in chicks. Eight-day-old male chicks were intracerebroventricularly injected with saline or the peptides. Water intake was measured 120 min after the injection under feed-deprived conditions. Intracerebroventricular administration of Met-enkephalin (a δ-opioid receptor agonist), β-endorphin (a δ-opioid receptor agonist), and nociception (a κ-opioid receptor and opioid receptor-like protein agonist) significantly suppressed water intake in chicks, whereas dynorphin B (a κ-opioid receptor agonist) and endomorphin-1 and 2 (μ-opioid receptor agonists) did not affect water intake. Intracerebroventricular administration of vasotocin, mesotocin, and CRF significantly suppressed water intake in chicks. Our findings suggest that none of the neuropeptides used in this study function as thirst-inducing peptides in the central nervous system of chicks.