ABSTRACT Central glutamate, melanocortin and corticotropin systems have mediatory role on several physiologic functions in the brain, but their interactions on appetite regulation are not fully elicited. So, the aim of the current study was to determine interaction of the glutamate with melanocortin and corticotropin systems on food intake in 3-h food-deprived (FD3) neonatal meat-type chicken. In experiment 1, chicken intracerebroventricular (ICV) injected (A) phosphate-buffered saline (PBS), (B) glutamate (75 nmol), (C) glutamate (150 nmol) and (D) glutamate (300 nmol). In experiment 2, (A) PBS, (B) astressin-B (CRF1/CRF2 receptors antagonist, 30 µg), (C) glutamate (300 nmol) and (D) astressin-B+glutamate were ICV injected. Experiments 3-5 were similar to experiment 2, except birds were injected with astressin2-B (CRF2 receptor antagonist, 30 µg), SHU9119 (MC3/MC4 receptor antagonist, 0.5 nmol) and MCL0020 (MC4 receptor antagonist, 0.5 nmol) instead of the astressin-B. In experiment 6, the injections were (A) PBS, (B) MTII (MC3/MC4 receptor agonist, 2.5ng), (C) glutamate (75nmol) and (D) MTII+glutamate. Then, cumulative feed intake was recorded at 30, 60 and 120 minutes after injection. According to the results, dose dependent hypophagia observed by ICV injection of the glutamate (75, 150 and 300nmol) compared to control group in neonatal broiler chicken (p<0.05). Co-injection of the astressin-B+glutamate and astressin2-B+glutamate decreased glutamate-induced hypophagia in neonatal broiler chicken (p<0.05). Co-injection of the glutamate+MC3/MC4 receptors antagonist decreased hypophagic effect of the glutamate (p<0.05). These results suggested hypophagic effect of the glutamate mediates via CRF1/CRF2 and MC3/MC4 receptors in chickens.

ABSTRACT The present study was designed to examine the role of Opioidergic and Histaminergic systems on feeding behavior in 3-hour food deprived neonatal meat- type chicks. In experiment 1, chicks received intracerebroventricular (ICV) injection of (A) control solution, (B) α-FMH (alpha fluoromethyl histidine; 250 nmol), (C) DAMGO (µ-opioid receptor agonist, 125 pmol) and (D) α-FMH + DAMGO. Experiments 2-4 were similar to experiment 1, except chicken ICV injected with Chlorpheniramine (histamine H1 receptors antagonist; 300 nmol), famotidine (histamine H2 receptors antagonist; 82 nmol) and Thioperamide (histamine H3 receptors antagonist; 300 nmol) instead of the α-FMH. In experiments 5-8, birds ICV injected with the same procedure as experiments 1-4, except they were injected with DPDPE (δ-opioid receptor agonist, 40 nmol) instead of DAMGO. Experiments 9-12 were similar to the experiments 1-4, except neonatal broilers ICV were injected with U-50488H (κ-opioid receptor agonist, 30 nmol) instead of DAMGO. Then the cumulative food intake was measured until 120 min post injection. According to the results, ICV injection of DAMGO, significantly decreased food intake (p<0.05) while DPDPE and U-50488H increased feeding behavior compared to the control group (p<0.05). Co-administration of the α-FMH and DAMGO significantly inhibited hypophagic effect of the DAMGO in neonatal broilers (p<0.05). Also, Chlorpheniramine significantly inhibited DAMGO- induced feeding behavior in neonatal chicks (p<0.05). In addition, co-administration of the Thioperamide + DAMGO significantly amplified the hypophagic effect of the DAMGO in neonatal chicks (p<0.05). However, famotidine had no effect on food intake induced by DAMGO (p>0.05). Also, the hyperphagic effect of DPDPE and U-50488 had no affect by α-FMH, Chlorpheniramine, famotidine and Thioperamide (p>0.05). These results suggested that an interconnection between central opioidergic and histaminergic systems on feeding behavior is mediated via µ-opioid and H1/H3 receptors in neonatal broilers.

ABSTRACT Feeding behavior is regulated via a complex network which interacts via diverse signals from central and peripheral tissues. Endocannabinoids modulate release of GABA in a variety of regions of the central nervous system. Endocannabinoids and GABAergic system have an important role in the central regulation of appetite. Thus, the present study examines the possible interaction of central canabinoidergic and GABAergic systems on food intake in 3-h food-deprived (FD3) neonatal layer-type chicks. The results of this study showed that intracerebroventricular (ICV) injection of 2-AG (2-Arachidonoylglycerol, selective CB1 receptors agonist, 2µg) significantly increased food intake and this effect of 2-AG was attenuated by Picrotoxin (GABAA antagonist, 0.5µg) (P<0.001); but 21ng CGP54626 (GABAB antagonist) had no effect (p>0.05). Also, hyperphagic effect of CB65 (CB2 receptors agonist, 1.25µg) was not affected by Picrotoxin or CGP54626 (p>0.05). Moreover, the food intake of chicks was significantly increased by ICV injection of GABAA agonist (Gaboxadol, 0.2 µg) and SR141716A (CB1 receptors antagonist, 6.25µg) significantly decreased Gaboxadol-induced hyperphagia (P<0.001) but CB2 receptors antagonist (AM630, 1.25µg) had no effect. In contrast, co-injection of SR141716A or AM630 with GABAB agonist (baclofen, 0.2µg) had no effect on the hyperphagia induced by baclofen (p>0.05). These data showed there might be an interaction between central cannabinoidergic and GABAergic systems via CB1 and GABAA receptors in control of food intake in neonatal layer chicks.