Elucidating the central anorexigenic mechanism of glucagon-like peptide 1 in Japanese quail (Coturnix japonica).

Glucagon-like peptide 1 (GLP-1) elicits a potent reduction in food intake, although the central mechanism mediating this appetite-suppressive effect is not fully understood in all species. To begin to elucidate the molecular mechanisms in quail, we administered GLP-1 via intracerebroventricular (ICV) injection to 7-day-old Japanese quail (Coturnix japonica) and determined effects on food and water intake, behavior, and brain nucleus activation. We observed a reduction in food and water intake, with the lowest effective dose being 0.01 nmol. Quail injected with GLP-1 displayed fewer steps, feeding pecks, exploratory pecks, and jumps, while time spent sitting increased. We quantified c-Fos immunoreactivity at 60 min post-injection in hypothalamic and brainstem nuclei that mediate food intake and determined that the hypothalamic paraventricular nucleus (PVN), and nucleus of the solitary tract and area postrema of the brainstem were activated in response to GLP-1. In conclusion, these results suggest that GLP-1 induces anorexigenic effects that are likely mediated at the level of the PVN and brainstem.

The anorexigenic effect of neuropeptide AF in Japanese quail, Coturnix japonica, is associated with activation of the melanocortin system.

Neuropeptide AF (NPAF) decreases food and water intake in birds and food intake in mammals. In this study, the objective was to determine the effects of centrally administered NPAF on food and water intake, hypothalamic c-Fos immunoreactivity and hypothalamic mRNA abundance of appetite-regulating factors in Japanese quail (Coturnix japonica). Seven days post hatch, 6 h fasted quail were intracerebroventricularly (ICV) injected with 0 (vehicle), 4, 8, or 16 nmol of NPAF and food and water intake were measured at 30 min intervals for 180 min. In Experiment 1, chicks which received 4, 8, and 16 nmol ICV NPAF had reduced food intake for 120, 60 and 180 min following injection, respectively, and reduced water intake during the entire 180 min observation. In Experiment 2, there was increased c-Fos immunoreactivity in the paraventricular nucleus, the ventromedial nucleus of the hypothalamus, and the dorsomedial hypothalamic nucleus in NPAF-injected quail. In Experiment 3, ICV NPAF was associated with decreased corticotropin-releasing factor mRNA, and an increase in hypothalamic proopiomelanocortin and melanocortin receptor 4 mRNA. These results demonstrate that central NPAF suppresses food and water intake in quail, effects that are likely mediated via the melanocortin system in the hypothalamus.

Reduced food intake during exposure to high ambient temperatures is associated with molecular changes in the nucleus of the hippocampal commissure and the paraventricular and arcuate hypothalamic nuclei.

Exposure to high ambient temperatures (HAT) is associated with increased mortality, weight loss, immunosuppression, and metabolic malfunction in birds, all of which are likely downstream effects of reduced food intake. While the mechanisms mediating the physiological responses to HAT are documented, the neural mechanisms mediating behavioral responses are poorly understood. The aim of the present study was thus to investigate the hypothalamic mechanisms mediating heat-induced anorexia in four-day old broiler chicks. In Experiment 1, chicks exposed to HAT reduced food intake for the duration of exposure compared to controls in a thermoneutral environment (TN). In Experiment 2, HAT chicks that were administered an intracerebroventricular (ICV) injection of neuropeptide Y (NPY) increased food intake for 60 min post-injection, while TN chicks that received NPY increased food intake for 180 min post-injection. In Experiment 3, chicks in both the TN and HAT groups that received ICV injections of corticotropin-releasing factor (CRF) reduced food intake for up to 180 min post-injection. In Experiment 4, chicks that were exposed to HAT and received an ICV injection of astressin ate the same as controls in the TN group. In Experiment 5, chicks exposed to HAT that received an ICV injection of α-melanocyte stimulating hormone reduced food intake at both a high and low dose, with the low dose not reducing food intake in TN chicks. In Experiment 6, there was increased c-Fos expression in the hypothalamic paraventricular nucleus (PVN), lateral hypothalamic area (LHA), and the nucleus of the hippocampal commissure (NHpC). In Experiment 7, exposure to HAT was associated with decreased CRF mRNA in the NHpC, increased CRF mRNA in the PVN, and decreased NPY mRNA in the arcuate nucleus (ARC). In sum, these results demonstrate that exposure to HAT causes a reduction in food intake that is likely mediated via downregulation of NPY via the CRF system.

Gastrin releasing peptide-induced satiety is associated with hypothalamic and brainstem changes in chicks.

Gastrin releasing peptide (GRP) is involved in the stimulation of gastric acid release from the stomach. It also mediates effects on feeding behavior. It is associated with anorexigenic effects in both mammalian and avian species, but the mechanism of action is unknown in any species. The aim of the present study was thus to investigate the hypothalamic and brainstem mechanisms mediating GRP-induced satiety in chicks. In Experiment 1, chicks that received intracerebroventricular (ICV) injection of GRP reduced food intake for up to 150 min following injection and reduced water intake up to 120 min following injection. In Experiment 2, chicks that were food restricted following GRP injection did not reduce water intake. Alimentary canal transit time was not affected by GRP in Experiment 3. A behavior analysis was conducted in Experiment 4, revealing that GRP-treated chicks reduced feeding pecks. In Experiment 5, GRP-treated chicks had increased c-Fos immunoreactivity in the lateral hypothalamus, paraventricular nucleus, and arcuate nucleus of the hypothalamus, and the nucleus of the solitary tract. Collectively, these results demonstrate that central GRP causes anorexigenic effects that are associated with hypothalamic changes without affecting other behaviors.