Interconnection between Adrenergic and Dopaminergic Systems in Feeding Behavior in Neonatal Chicks.

The current study was conducted to investigate the interaction between the central adrenergic and histaminergic systems and the broiler chick's feed intake. In the first experiment, the intracerebroventricular (ICV) injection of solutions was conducted which included 10 nmol of prazosin (an α1-receptor antagonist), 300 nmol of histamine, co-injection of prazosin and histamine. Experiments two to five were conducted similarly the same as the first experiment, in which chickens were ICV injected with 13 nmol of yohimbine (an α2-receptor antagonist), 24 nmol of metoprolol (a β1 adrenergic receptor antagonist), 5 nmol of ICI 118,551 (a β2 adrenergic receptor antagonist), and 20 nmol of SR 59230R (a β3 adrenergic receptor antagonist). The injected solutions in the sixth experiment included 300 nmol of noradrenaline, 250 nmol of α-FMH (an alpha fluoromethyl histidine), noradrenaline, and α-FMH. Seventh to ninth experiments were similar to the sixth experiment, except that the chickens were ICV injected with 300 nmol of chlorpheniramine (a histamine H1 receptors antagonist), 82 nmol of famotidine (a histamine H2 receptors antagonist), and 300 nmol of thioperamide (a histamine H3 receptors antagonist), rather than α-FMH. Afterward, the cumulative food intake was measured 120 min after injection. Based on the obtained results, both histamine ICV injection and noradrenaline injection reduced food intake (P<0.05). Moreover, co-injection of histamine and ICI 118,551 (P<0.05), and co-injection of noradrenaline and Chlorpheniramine reduced food intake (P<0.05). In addition, noradrenaline and Thioperamide co-injection improved hypophagic effect of noradrenaline in neonatal chicken (P<0.05). These findings suggested the effect of interconnection between adrenergic and histaminergic systems, which may be mediated by H1 and H3 histaminergic and β2 adrenergic receptors, on the regulation of food intake in the neonatal broiler chicken.

The information emerging from the studies demonstrates adrenergic system and nociceptin/orphanin FQ (N/OFQ) play a crucial role on appetite regulation but there is no information for their interaction. The purpose of this study was to examine the effects of intracerebroventricular (ICV) injection of prazosin (α1 receptor antagonist), yohimbine (α2 receptor antagonist), metoprolol (β1 adrenergic receptor antagonist), ICI 118,551 (β2 adrenergic receptor antagonist) and SR59230R (β3 adrenergic receptor antagonist) on N/OFQ-induced hyperphagia by 3-h food-deprived neonatal broiler chicken. In experiment 1, chicken injected with saline, prazosin (10 nmol), N/OFQ (16 nmol) and co-injection of prazosin + N/OFQ. In experiment 2, ICV injection of saline, yohimbine (13 nmol), N/OFQ (16 nmol) and yohimbine + N/OFQ applied to the birds. In experiment 3, injections were saline, metoprolol (24 nmol), N/OFQ (16 nmol) and metoprolol + N/OFQ. In experiment 4, the birds received ICV injection of saline, ICI 118,551 (5 nmol), (C) N/OFQ (16 nmol) and co-administration of ICI 118,551 + N/OFQ. In experiment 5, chicken injected with saline, SR59230R (20 nmol), N/OFQ (16 nmol) and SR59230R + N/OFQ. Then, cumulative food intake was recorded until 120 min after injection. According to the results, ICV injection of N/OFQ significantly increased food intake (P 0.05). These results suggest that the effect of N/OFQ on cumulative food intake is mediated via β2 adrenergic receptors in neonatal chicken.

Nowadays inquiry of possible interplay between different neurotransmitters in brain function is one of the major fields of interest for researchers. In the current study, we aimed to survey interaction between glutamatergic and nitrergic systems on food intake in layers. In this regards, total of 308 one-day-old female layer-type chicks divided to 28 groups of 11 individuals in 7 defined experiments. All chickens were kept 3 h food deprived and used for intracerebroventricular (ICV) injection in the 5 day olds. In experiments 1–5, treatment groups received ICV injection of 10 µl control solution, l-arginine (precursor of NO synthesis; 800 nmol). In addition, birds administrated by different antagonists of glutamatergic receptors including MK-801 (NMDA receptor antagonist; 15 nmol), CNQX (AMPA/kainate receptor antagonist; 390 nmol), AIDA (mGLUR1 glutamate receptor antagonist; 2 nmol), LY341495 (mGLUR2 glutamate receptor antagonist; 150 nmol), UBP1112 (mGLUR3 glutamate receptor antagonist; 2 nmol) besides combination of mentioned antagonists of glutamatergic receptors + l-arginine (800 nmol). In the experiment 6, groups injected by control solution, glutamate (300 nmol), l-NAME (100 nmol) besides combination of both drugs. In the experiment 7, birds were ICV injected by control solution, glutamate (75 nmol), l-arginine (200 nmol) and combination of glutamate + l-arginine. Then cumulative food intake measured as following a known amount of a diet was given to the animals after 30, 60 and 120 min post injection. Based on the results, administration of MK-801 (15 nmol) significantly attenuated hypophagic effect induced by l-arginine (800 nmol) in neonatal chicks (P 0.05). Furthermore, co-administration of sub-effective doses of glutamate with l-arginine made significant hypophagic effect in comparison with control group and any of treatment group, which received sole glutamate or only l-arginine (P < 0.05). As a conclusion, it seems central glutamatergic system is modulating hypophagic effect induced by nitrergic system through NMDA receptor in neonatal layer chicks. Apparently, l-arginine and glutamate neurotransmitters showed synergistic effect on regulating food intake in layers.

Objective: The aim of the current study was to determine the possible interaction of the central leptin and Glutamatergic systems on feeding behavior in neonatal 3-hours food deprived (FD3) broilers chickens.Methods: In experiment 1, FD3 chicken received intracerebroventricular (ICV) injection of control solution (group i) and 2.5, 5 and 10 µg of Leptin (groups ii–iv). In experiment 2, FD3 chicken were ICV injected with (group i) control solution and groups ii–iv with 2.5, 5 and 10 nmol of AG-490 (JAK2 antagonist). In experiment 3, injections were (i) control solution, (ii) Leptin (10 µg), (iii) AG-490 (2.5 nmol) and (iv) Leptin + AG-490. In experiment 4, broiler chickens were ICV injected with (i) control solution, (ii) Leptin (10 µg), (iii) MK-801 (NMDA glutamate receptors antagonist; 15 nmol) and (iv) Leptin + MK-801. Experiments 5–9 were similar to experiment 1, except chicken were ICV injected with CNQX (AMPA receptor antagonist, 390 nmol), UBP-302 (Kainate receptor antagonist, 390 nmol), AIDA (mGluR1 antagonist, 2 nmol), LY341495 (mGluR2 antagonist, 150 nmol) and UBP1112 (mGluR3 antagonist, 2 nmol) instead of MK-801. Then, food intake was measured until 120 min after injection.Results: ICV injection of leptin (2.5, 5 and 10 µg) significantly decreased food intake in a dose dependent manner (p < 0.05). Also, ICV injection of the JAK2 antagonist (2.5, 5 and 10 nmol) had hyperphagic effect in chicken (p < 0.05). Co-administration of leptin + AG-490, partially decreased leptin-induced hypophagia in broiler chicken (p < 0.05). In addition, co-injection of leptin + MK-801 significalty inhibited leptin-induced hypophagia in neonatal chicken (p < 0.05). Also, co-administration of leptin + CNQX partially attenuated hypophagic effect of leptin in chicken (p < 0.05).Conclusion: The results of present study suggest that leptin has hypophagic effect in neonatal chicken and this effect is probably mediated via NMDA and AMPA glutamatergic receptors.

ABSTRACT1. 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.

Oxytocin neurons have a physiological role in food intake and energy balance. Several studies have shown that central histaminergic and adrenergic systems synapse on oxytocin neurons but there is no information for their interaction on food intake regulation in birds. The purpose of this study was to examine the effects of intracerebroventricular (ICV) injection of α-fluoromethylhistidine (α-FMH, histidine decarboxylase inhibitor), chlorpheniramine (histamine H1 receptors antagonist), famotidine (histamine H2 receptors antagonist), thioperamide (histamine H3 receptors antagonist), prazosin (α1 receptor antagonist), yohimbine (α2 receptor antagonist), metoprolol (β1 adrenergic receptor antagonist), ICI 118,551 (β2 adrenergic receptor antagonist) and SR59230R (β3 adrenergic receptor antagonist) on oxytocin-induced hypophagia in 3-h food-deprived (FD3) neonatal broiler chicken. In Experiment 1, 3h-fasted chicks were given an ICV injection of saline, α-FMH (250nmol), oxytocin (10μg) and co-injection of α-FMH+oxytocin. Experiments 2-9 were similar to experiment 1 except birds were injected with chlorpheniramine (300nmol), famotidine (82nmol), thioperamide (300nmol), prazosin (10nmol), yohimbine (13nmol), metoprolol (24nmol), ICI 118,551(5nmol) and SR59230R (20nmol) instead of α-FMH, respectively. After injection cumulative food intake was measured until 120min post injection. According to the results, ICV injection of oxytocin significantly decreased food intake in broiler chickens (P<0.001). ICV injection of α-FMH significantly attenuated hypophagic effect of oxytocin (P<0.001). Also, co-injection of chlorpheniramine plus oxytocin significantly decreased the effect of oxytocin on food intake (P<0.001). Co-administration of thioperamide and oxytocin significantly amplified hypophagic effect of oxytocin in chickens (P<0.001). In addition, ICI 118,551 attenuated hypophagic effect of oxytocin (P<0.001); while famotidine, prazosin, yohimbine, metoprolol and SR59230R had no effect on oxytocin- induced food intake in FD3 broiler chickens. These results suggest that the effect of oxytocin on food intake is probably mediated by histaminergic (via H1 and H3 receptors) and noradrenergic (via β2 receptors) systems in broiler chickens.

This study purposed to discover the connection between the central glutamatergic and histaminergic systems on feeding behavior in layer chickens. In the first experiment, chicks obtained intracerebroventricular (ICV) injections of saline (control solution), α-FMH (250 nmol), glutamate (300 nmol), and α-FMH + glutamate. Experiments 2-6 were comparable to the first experiment, apart from the birds being injected with chlorpheniramine (histamine H1 receptor antagonist, 300 nmol), famotidine (histamine H2 receptor antagonist, 82 nmol), and thioperamide (histamine H3 receptor antagonist, 300 nmol) instead of α-FMH. In Experiment five, experimental groups were divided into (A) control solution, (B) MK-801 (N-methyl-D-aspartate receptor antagonist, 15 nmol), (C) histamine (300 nmol) and (D) MK-801 + histamine. Experiments 6-10 and Experiment five were similar apart from the ICV injections of CNQX (AMPA receptor antagonist, 360 nm), UBP-302 (Kainate receptor antagonist, 390 nm), AIDA (mGluR1 antagonist, 2 nmol), LY341495 (mGluR2 antagonist, 150 nmol), and UBP1112 (mGluR3 antagonist, 2 nmol) given instead of MK-801. Afterward, cumulative food intake was recorded at30, 60, and 120 minutes after the injection process. According to the results, ICV injection of glutamate considerably reduced food intake (p<0.05). Co-injection of α-FMH + glutamate and/or chlorpheniramine + glutamate reduced the hypophagic influence of glutamate (p<0.05), whereas thioperamide + glutamate augmented glutamate-induced hypophagia in neonatal chicks (p<0.05). Co-injection of MK-801 + histamine or UBP-302 + histamine reduced the hypophagic influence of the histamine (p<0.05), whereas LY341495 + histamine augmented the hypophagic influence of the histamine (p<0.05). Given the results, it is suggested that the effect of the connection between these systems on the process of food intake regulation is mediated by H1 and H3 histamines as well as NMDA, Kainate, and mGluR2 glutamate receptors in neonatal layer chickens.

Furuse, M., Bungo, T., Ao, R., Ando, R., Shimojo, M., Masuda, Y. and Denbow, D.M. 2000. Involvement of central gastrin and cholecystokinin in the regulation of food intake in the neonatal chick. J. Appl. Anim. Res., 18: 129–136. The effects of intracerebroventricular (ICV) injection of chicken gastrin and cholecystokinin (CCK) on food intake were compared in the neonatal chick. In Experiment 1, the effect of 131 pmol of chicken gastrin (36 amino acid residues) on food intake was compared with 66 and 131 pmol of CCK-8S over 2h. Chicken gastrin strongly inhibited food intake, but both levels of CCK-8S did not. The similar effect of 131 pmol chicken gastrin was obtained by 262 pmol CCK-8S at Ih after ICV injection in Experiment 2. This suppressive effect of chicken gastrin continued over 2h after ICV injection, though the effect of CCK-8S had disappeared by 2h. In Experiment 3, the effects of 131 pmol of CCK-8S, CCK-33S and chicken gastrin were compared. The effect of CCK-8S was weak, but CCK-33S and chickengastrin similarly and strongly inhibited food intake of chicks. These results suggested that the suppressive effect of food intake of gastrin/CCK family may be dependent upon the length of amino acid sequence.

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.

Recently, methylamine has been found as an endogenous amine, which is controlling food intake in mammals. However, there is no evidence about the effect of methylamine on feeding behavior in poultry. So, the present study was designed to evaluate the effect of intracerebroventricular (ICV) injection of methylamine and involvement of central methylamine/dopaminergic systems on feeding behavior in neonatal meat type chicks. In experiment 1, chicks were ICV injected with different doses of methylamine (0.48, 0.96, 1.44, 1.92 and 2.40 μmol). In experiment 2, chicks received a dose of either the control solution, 2.40 μmol methylamine, 125 nmol L-DOPA (dopamine precursor) or a combination of methylamine plus L-DOPA. Experiments 3-7 were similar to experiment 2 except that 150 nmol 6-OHDA (dopamine synthase inhibitor), 5 nmol SCH23390 (D1 receptor antagonist), 5 nmol AMI-193 (D2 receptor antagonist), 6.4 nmol NGB2904 (D3 receptor antagonist) and 6 nmol L-741, 742 (D4 receptor antagonist) were used instead of 125 nmol L-DOPA, respectively. Cumulative food intake was determined until 2 h post-injection. According to the results, methylamine significantly decreased food intake in a dose dependent manner (p < 0.05). The inhibitory effect of methylamine on food intake was significantly attenuated by 6-OHDA, SCH23390 and AMI-193 (P < 0.05), but NGB2904 and L-741, 742 had no effect on food intake induced by methylamine. In addition, hypophagic effect of methylamine significantly amplified by L-DOPA (P < 0.05). These results suggest that methylamine decrease food intake and there is an interaction between methylamine and dopaminergic system via D1 and D2 receptors in chickens.

Adrenomedullin has various physiological roles including appetite regulation. The objective of present study was to determine the effects of ICV injection of adrenomedullin and its interaction with NPY and CCK receptors on food intake regulation. In experiment 1, chickens received ICV injection of saline and adrenomedullin (1, 2, and 3 nmol). In experiment 2, birds injected with saline, B5063 (NPY1 receptor antagonist, 1.25 µg), adrenomedullin (3 nmol) and co-injection of B5063+adrenomedullin. Experiments 3 to 5 were similar to experiment 2 and only SF22 (NPY2 receptor antagonist, 1.25 µg), SML0891 (NPY5 receptor antagonist, 1.25 µg) and CCK4 (1 nmol) were injected instead of B5063. In experiment 6, ICV injection of saline and CCK8s (0.125, 0.25, and 0.5 nmol) were done. In experiment 7, chickens injected with saline, CCK8s (0.125 nmol), adrenomedullin (3 nmol) and co-injection of CCK8s+adrenomedullin. After ICV injection, birds were returned to their individual cages immediately and cumulative food intake was measured at 30, 60, and 120 min after injection. Adrenomedullin (2 and 3 nmol) decreased food intake compared to control group (P < 0.05). Coinjection of B5063+adrenomedullin amplified hypophagic effect of adrenomedullin (P < 0.05). The ICV injection of the CCK8s (0.25 and 0.5 nmol) reduced food intake (P < 0.05). Co-injection of the CCK8s+adrenomedullin significantly potentiated adrenomedullin-induced hypophagia (P < 0.05). Administration of the SF22, SML0891 and CCK4 had no effect on the anorexigenic response evoked by adrenomedullin (P > 0.05). These results suggested that the hypophagic effect of the adrenomedullin is mediated by NPY1 and CCK8s receptors. However, our novel results should form the basis for future experiments.

The aim of the current study was to investigate the interaction of the nitric oxide and cannabinoidergic systems on feeding behaviour in neonatal chicken.A total of 6 experiments were designed to evaluate the interaction between cannabinoidergic and nitrergic systems on food intake in 3-h food-deprived (FD3) neonatal chickens. In Experiment 1, chickens received intracerebroventricular (ICV) injections of saline, 2-arachidonoylglycerol (2-AG) (a CB1 receptor agonist, 2 µg), l-arginine (nitric oxide precursor, 200 nmol) and co-administration of 2-AG + l-arginine. In Experiment 2, ICV injection of saline, 2-AG (2 µg), l-NAME (a nitric oxide synthesis inhibitor, 100 nmol) and their combination (2-AG + l-NAME) were applied to the birds. In Experiment 3, injections were saline, CB65 (a CB2 receptor agonist, 1.25 µg), l-arginine (200 nmol) and CB65 + l-arginine. In Experiment 4, birds received ICV injection of saline, CB65 (1.25 µg), l-NAME (100 nmol) and CB65 + l-NAME. In Experiment 5, chickens were ICV injected with saline, l-arginine (800 nmol), SR141716A (a selective CB1 receptor antagonist, 6.25 µg) and l-arginine + SR141716A. In Experiment 6, birds were injected with saline, l-arginine (800 nmol), AM630 (a selective CB2 receptor antagonist, 5 µg) and l-arginine + AM630. Cumulative food intake was recorded until 2-h post injection.ICV injection of CB1 and CB2 receptor agonists increased food intake. Co-injection of 2-AG + l-NAME increased the hyperphagic effects of CB1 receptors. CB2 receptor-induced food intake was not affected by co-administration of CB65 + l-NAME. l-Arginine decreased food intake and this effect was amplified by co-injection of l-arginine + SR141716A. However; CB2 receptor antagonists had no effect on l-arginine-induced hypophagia.The results suggest that there is an interaction between endogenous nitric oxide and the cannabinoidergic system on feeding behaviour which is mediated via CB1 receptors in the neonatal chicken.

Melanocortin 3 and 4 receptors (MC3R and MC4R) are known as the main receptors for melanocortin-induced hypophagia in mammalian and poultry. Also, central glutamatergic system has mediatory role on function of the melanocortin system in some brain areas. So, the aim of the current study was to determine the role of MC3/MC4 receptors agonist on food intake and its interaction with glutamatergic in 3-h food-deprived (FD3) neonatal broilers. In experiment 1, chickens were intracerebroventricular (ICV) injected with control solution, MTII (MC3/MC4 receptors agonist; 2.45, 4.8 and 9.8pmol). In experiment 2, control solution, SHU9119 (MC3/MC4 receptors antagonist; 0.5, 1 and 2nmol) were ICV injected. In experiment 3, birds ICV injected with control solution, SHU9119 (0.5nmol), MTII (9.8pmol) and co-injection of the SHU9119+MTII. Experiments 4-8 were similar to experiment 3, except birds injected with MK-801 (NMDA glutamate receptors antagonist, 15nmol), CNQX (AMPA glutamate receptors antagonist; 390nmol), AIDA (mGLUR1 glutamate receptors antagonist; 2nmol), LY341495 (mGLUR2 glutamate receptors antagonist; 150nmol) and UBP1112 (mGLUR3 glutamate receptors antagonist; 2nmol) instead of SHU9119. Then, cumulative food intake was recorded until 120min after injection. According to the results, dose dependent hypophagia observed after ICV injection of the MTII (p<0.05). ICV injection of SHU9119 significantly increased food intake in birds (p<0.05). Co-injection of SHU9119+MTII significantly inhibited MTII- induced hypophagia in neonatal chicks (p<0.05). In addition, hypophagia- induced by MTII was significantly attenuated with co-injection of MTII+MK-801(p<0.05). These results suggested MC3 and MC4 receptors have inhibitory role on food intake and this effect is probably mediated by NMDA glutamate receptors in neonatal chickens.

The aim of the current study was to determine possible interaction of central oxytocin and opioidergic system on food intake regulation in neonatal layer-type chicken. In experiment 1, FD3 chicken ICV injected with control solution, oxytocin (10 µg), β-FNA (µ receptor antagonist, 5 µg) and oxytocin (10 µg) + β-FNA were injected. Experiments 2–6 were similar to experiments 1, except chicken injected with nor-BNI (κ receptor antagonist, 5 µg), NTI (δ receptor antagonist, 5 µg), DAMGO (µ receptor agonist, 62.25 pmol), U-50488H (κ receptor agonist, 10 nmol), DPDPE (δ receptor agonist, 20 pmol) instead of β-FNA. In experiment 7, control solution, DAMGO (125 pmol), d(CH2)5Tyr(Me)-[Orn8]-vasotocin (oxytocin antagonist, 5 µg) and DAMGO + d(CH2)5Tyr(Me)-[Orn8]-vasotocin were ICV injected to FD3 chicken. Experiments 8 and 9 were similar to experiments 7, except chicken injected with U-50488H (30 nmol) and DPDPE (40 pmol) instead of DAMGO. Then, cumulative food intake was recorded at 30, 60 and 120 min after injection. According to the results, ICV injection of the oxytocin (10 µg) significantly decreased food intake compared to control group (P < 0.05). Co-injection of the oxytocin + β-FNA and oxytocin + U-50488H significantly decreased hypophagic effect of the oxytocin (P < 0.05). While, co-injection of the oxytocin + nor-BNI or oxytocin + DAMGO significantly amplified hypophagic effect of the oxytocin in chicken (P < 0.05). In addition, ICV injection of DAMGO (125 pmol) significantly decreased cumulative food intake compared to control group (P < 0.05). However, co-addministration of the DAMGO + (CH2)5Tyr(Me)-[Orn8]-vasotocin significantly decreased hypophagic effect of the DAMGO (P < 0.05) in chicken. These results suggested there are interconnection between oxytocin and opioidergic system on central food intake regulation, which mediates via µ and κ opioidergic receptors in neonatal layer-type chicken.

ABSTRACT1. The present study was conducted to investigate whether brain somatostatin increases feed intake in neonatal chickens. The mediating role of neuropeptide Y receptors on feed intake induced by somatostatin was investigated.2. In this study, seven experiments were designed, each with four treatment groups (n = 44 in each experiment). In Experiment 1, chicks received control solution and 0.5, 1 and 2 nmol of somatostatin through intracerebroventricular (ICV) injection. In experiments 2, 3 and 4, chickens were ICV injected with control solution and 1.25, 2.5 and 5 μg of B5063 (NPY1 receptor antagonist), SF22 (NPY2 receptor antagonist) and SML0891 (NPY5 receptor antagonist), respectively. In experiment 5, 6 and 7 chickens received ICV injection of B5063, SF22, SML0891, with a co-injection of + somatostatin, control solution and somatostatin. The cumulative feed intake was measured until 120 min post injection.3. Somatostatin significantly increased feed intake in FD3 chicks. Both B5063 and SML0891 dose-dependently decreased feed intake compared with the control group, while SF22 led to a dose-dependent increase in feed intake. In addition, the hyperphagic effect of somatostatin significantly decreased with co-injection of B560 plus somatostatin (p < 0.05), but SF22 and SML0891 had no effect on feed intake induced by somatostatin in chicks (p > 0.05).4. Based on the results of this study, it is likely that somatostatin increased feed intake and NPY1 receptor acts as a mediator in hyperphagic effect of somatostatin in neonatal chicks.