Food Intake In Neonatal Chicks Research Articles

Central Interaction Between L-Ornithine and Neuropeptide Y in the Regulation of Feeding Behavior of Neonatal Chicks.

Ornithine has been identified as a potential satiety signal in the brains of neonatal chicks. We hypothesized that brain nutrient signals such as amino acids and appetite-related neuropeptides synergistically regulate food intake. To test this hypothesis, we investigated the interaction between neuropeptide Y (NPY) and ornithine in the control of feeding behavior in chicks and the associated central and peripheral amino acid metabolic processes. Five-day-old chicks were intracerebroventricularly injected with saline, NPY (375 pmol), or NPY plus ornithine (2 or 4 μmol) at 10 μl per chick, and then subjected to ad libitum feeding conditions; food intake was monitored for 30 min after injection. Brain and plasma samples were collected after the experiment to determine free amino acid concentrations. Co-injection of NPY and ornithine significantly attenuated the orexigenic effect induced by NPY in a dose-dependent manner. Central NPY significantly decreased amino adipic acid, asparagine, γ-aminobutyric acid, leucine, phenylalanine, tyrosine, and isoleucine levels, but significantly increased lysine levels in the brain. Co-injection of NPY and ornithine significantly increased ornithine and proline levels in all examined brain regions, but decreased diencephalic tryptophan and glycine levels compared with those of the control and NPY-alone groups. Co-injection of NPY and high-dose ornithine significantly decreased methionine levels in all brain regions. Central NPY significantly suppressed the plasma concentrations of amino acids, including proline, asparagine, methionine, phenylalanine, tyrosine, leucine, isoleucine, glycine, glutamine, alanine, arginine, and valine, and this reduction was greater when NPY was co-injected with ornithine. These results suggest that brain ornithine interacts with NPY to regulate food intake in neonatal chicks. Furthermore, central NPY may induce an anabolic effect that is modified by co-injection with ornithine.

Central GABAA receptor mediates taurine-induced hypothermia and possibly reduces food intake in thermo-neutral chicks and regulates plasma metabolites in heat-exposed chicks.

The aim of this study was to examine the central action of taurine on body temperature and food intake in neonatal chicks under control thermoneutral temperature (CT) and high ambient temperature (HT). Intracerebroventricular injection of taurine caused dose-dependent hypothermia and reduced food intake under CT. The mRNA expression of the GABAA receptors, GABAAR-α1 and GABAAR-γ, but not that of GABABR, significantly decreased in the diencephalon after central injection of taurine. Subsequently, we found that picrotoxin, a GABAAR antagonist, attenuated taurine-induced hypothermia. Central taurine significantly decreased the brain concentrations of 3-methoxy-4-hydroxyphenylglycol, a major metabolite of norepinephrine; however, the concentrations of serotonin, dopamine, and the epinephrine metabolites, 3,4-hydroxyindoleacetic acid and homovanillic acid, were unchanged. Although hypothermia was not observed under HT after central injection of taurine, plasma glucose and uric acid levels were higher, and plasma sodium and calcium levels were lower, than those in chicks under CT. In conclusion, brain taurine may play a role in regulating body temperature and food intake in chicks through GABAAR. The changes in plasma metabolites under heat stress suggest that brain taurine may play an important role in maintaining homeostasis in chicks.

Interactive effects of peripheral and central administration of LPS with inhibition of CRF receptors on food intake in neonatal chicks

Anorexia is a part of the acute phase response (APR). Lipopolysaccharide (LPS) is frequently used to mimic APR and induces anorexia. The mechanism underlying anorexia associated with APR in chicks is not well understood. In the present study, the possible involvement of corticotrophin-releasing factor (CRF) on anorexic effects of LPS in neonatal chicks was investigated. For this aim, different doses of LPS were administrated via both intracerebroventricular (ICV) and intraperitoneal (IP) routes in order to assess its effects on chick’s food intake. Subsequently, the effect of ICV injection of astressin, a CRF receptor antagonist, on anorexia induced by ICV and IP administration of LPS was investigated. Food intake was significantly decreased following either central or systemic administration of LPS. ICV co -injection of astressin and LPS significantly diminished anorexic effects of central LPS. However, anorexia induced by peripheral LPS was not attenuated by central injection of astressin. These data indicated that the brain CRF receptors are involved in central LPS-induced anorexia in chicks.

Central Opioidergic System Interplay with Histamine on Food Intake in Neonatal Chicks: Role of µ-Opioid and H1/H3 Receptors

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). 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.

The effect of Nesfatin-1 on food intake in neonatal chicks: role of CRF1 /CRF2 and H1/ H3 receptors.

The present study was designed to determine the effect of central injection of Nesfatin-1 and corticotropin and histaminergic systems on food intake in neonatal meat-type chicks. In this study, 7 experiments were designed, each with 4 treatment groups. In experiment 1, four groups of chicks received the ICV injection of (A) phosphate-buffered saline (PBS), (B) Nesfatin-1 (10ng), (C) Nesfatin-1 (20ng) and (D) Nesfatin-1 (40ng). In experiment 2, (A) PBS, (B) Astressin-B (CRF1/CRF2 receptors antagonist; 30µg), (C) Nesfatin-1 (40ng) and (D) Nesfatin-1 + Astressin-B were injected. In experiments 3-6, chicken received ICV injection of the Astressin2-B (CRF2 receptor antagonist; 30µg), α-FMH (alpha fluoromethyl histidine; as inhibitor of histidine decarboxylase, 250nmol), Chlorpheniramine (histamine H1 receptors antagonist, 300nmol), Famotidine (histamine H2 receptors antagonist, 82nmol) and Thioperamide (histamine H3 receptors antagonist, 300nmol) instead of the Astressin-B. Then the cumulative food intake measured until 120min post-injection. According to the results, ICV injection of Nesfatin-1 dose dependently decreased food intake in neonatal chicks (P < 0.05). Co-injection of the Nesfatin-1 and Astressin-B (CRF1/CRF2) inhibited Nesfatin-1 induced hypophagia (P < 0.05). ICV inejction of the Nesfatin-1 + Astressin-B significantly inhibited the effect of Nesfatin-1 on food intake (P < 0.05). In addition, α-FMH and chlorpheniramine attenuated Nesfatin-1-induced hypophagia in chicks (P < 0.05); while thioperamide significantly amplified the effect of Nesfatin-1 on food intake in chicks (P < 0.05). These results suggested Nesfatin-1 has an anorectic effect in 3-hour food deprived neonatal meat-type chicks and this effect was mediated by corticotropin CRF1/CRF2 as well as histamine H1 and H3 receptors.

Interaction Between Central Oxytocinergic and Glutamatergic Systems on Food Intake in Neonatal Chicks: Role of NMDA and AMPA Receptors

The present study was designed to examine the interconnection between oxytocinergic and glutamatergic systems on feeding behavior in neonatal chicks. In experiment 1, FD3 chicken ICV injected with (A) saline (control solution), (B) oxytocin (10 µg), (C) MK-801(NMDA receptor antagonist, 15 nmol) and (D) oxytocin + MK-801. In experiment 2, (A) control solution, (B) oxytocin (10 µg), (C) CNQX (390 nmol) and (D) oxytocin + CNQX were injected. Experiments 3–6 were similar to experiment 1, except FD3 chicks ICV injected with CNQX (AMPA glutamate receptors antagonist, 390 nmol), AIDA (mGLUR1 glutamate receptors antagonist, 2 nmol), LY341495 (mGLUR2 glutamate receptors antagonist, 150 nmol) and UBP1112 (mGLUR3 glutamate receptors antagonist, 2 nmol) instead of MK-801, respectively. In experiment 7, injections were (A) control solution, (B) glutamate (300 nmol), (C) ABN-297 (9 nmol) and (D) glutamate + ABN-297. Then the cumulative food intake measured until 120 min post injection. According to the results, ICV injection of glutamate decreased food intake and co-injection of the glutamate + ABN-297 increased food consumption in neonatal broiler (P < 0.001). ICV injection of oxytocin, significantly decreased food intake in neonatal chicks (P < 0.001). Also, MK-801 significantly attenuated oxytocin- induced hypophagia in chicks (P < 0.001). In addition, combination of oxytocin plus CNQX significantly decreased hypophagic effect of the oxytocin in neonatal chicks (P < 0.001). These results suggested interconnection between central oxytocinergic and glutamatergic systems on feeding behavior is probably mediated via NMDA and AMPA receptors.

Interaction between central GABAA receptor and dopaminergic system on food intake in neonatal chicks: role of D1 and GABAA receptors

ABSTRACTObjective: The present study was designed to examine the role of central γ-Aminobutyric acidA receptors and dopaminergic system on feeding behaviour in neonatal layer-type chicken.Methods: In this study, six experiments were designed, each with four treatment groups (n = 44 in each experiment). In experiment 1, four groups of 3-h food-deprived chicks received a dose of either the intracerebroventricular injection of (1) control solution, (2) Levo-dihydroxyphenylalanine as precursor of dopamine; 125 nmol, (3) Gaboxadol (γ-Aminobutyric acidA receptor agonist, 0.2 µg) and (4) Levo-dihydroxyphenylalanine (125 nmol) plus Gaboxadol (0.2 µg). Experiments 2–6 were similar to experiment 1, except that the chickens were intracerebroventricular-injected with 6-hydroxydopamine (is a neurotoxin; 2.5 nmol), SCH23390 (D1 receptor antagonist, 5 nmol), AMI-193 (D2 receptor antagonist, 5 nmol), NGB2904 (D3 receptor antagonist, 6.4 nmol) and L-741,742 (D4 receptor antagonist, 6 nmol) instead of levo-dihydroxyphenylalanine. Then, the cumulative food intake was measured until 120 min post-injection.Results: According to the results, intracerebroventricular injection of Gaboxadol (0.2 µg) significantly increased the food intake (P < 0.05). Co-injection of the 6-hydroxydopamine + Gaboxadol significantly amplified the food intake (P < 0.05). Intracerebroventricular injection of SCH23390 (5 nmol) + Gaboxadol (0.2 µg) significantly amplified the Gaboxadol-induced hyperphagia (P < 0.05). No significant effect was observed by co-injection of the D2–D4 receptor antagonists + Gaboxadol (P > 0.05).Conclusion: These results suggested the interconnection between central Dopaminergic and γ-Aminobutyric acidA on the feeding behaviour mediates via D1 and γ-Aminobutyric acidA receptors in 3-h food-deprived neonatal layer-type chicken.

Interaction Between Central Opioidergic and Glutamatergic Systems on Food Intake in Neonatal Chicks: Role of NMDA, AMPA and mGLU1 Receptors

The present study was designed to examine the role of opioidergic and glutamatergic systems on feeding behavior in neonatal meat-type chicken. In experiment 1, FD3 neonatal broilers ICV injected with (A) saline, (B) DAMGO (µ-opioid receptor agonist, 125 pmol), (C) MK-801 (NMDA glutamate receptors antagonist, 15 nmol) and (D) combination of DAMGO plus MK-801. Experiments 2–5 were similar to experiment 1, except FD3 chicks ICV injected with CNQX (AMPA glutamate receptors antagonist, 390 nmol), AIDA (mGLU1 receptors antagonist, 2 nmol), LY341495 (mGLU2 receptors antagonist, 150 nmol) and UBP1112 (mGLU3 receptors antagonist, 2 nmol) instead of MK-801, respectively. In experiments 6–10, FD3 chicks ICV injected as the same as procedure to the experiments 1–5, except to inject with DPDPE (δ-opioid receptor agonist, 40 nmol) instead of the DAMGO. The experiments 11–15 were similar to the experiments 1–5, except neonatal broilers ICV injected with U-50488H (κ-opioid receptor agonist, 30 nmol) instead of DAMGO. Then the cumulative food intake 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-injection of the DAMGO + MK-801 and DAMGO + AIDA, significantly decreased DAMGO-induced hypophagia in neonatal chicks (P < 0.05). Also, co-injection of the DPDPE + CNQX significantly amplified DPDPE induced feeding behavior (P < 0.05). These results suggested interconnection between central opioidergic and glutamatergic systems on feeding behavior mediates via µ- and δ-opioid receptor with NMDA, AMPA and mGLU1 receptors in FD3 neonatal broilers. These findings may shed light on the circuitry underlying interconnection between central opioidergic and glutamatergic systems on feeding behavior.

L-Ornithine is a potential acute satiety signal in the brain of neonatal chicks

Recently, we observed that neonatal chicks exhibit feeding behavior characterized by frequent food intake and short resting intervals, with changes detected in the brain amino acid and monoamine concentrations. In this study, we aimed to clarify further the relationship between the appetite of neonatal chicks and brain amino acid metabolism. In Experiment 1, changes were investigated in free amino acids in the brain under conditions of regulated appetite induced by fasting and subsequent short-term re-feeding. Chicks (5days old) were distributed into four treatment groups — namely, fasting for 3h, and fasting for 3h followed by re-feeding for 10, 20 or 30min. Brain samples were collected after treatment to analyze free amino acid concentrations. Amino adipic acid and proline in all brain parts as well as arginine and ornithine in all brain parts – except mesencephalic arginine and cerebellar ornithine – were increased in a time-dependent manner following re-feeding. In Experiment 2, we further examined the effect of exogenous administration of some amino acids altered in association with feeding behavior in Experiment 1. We chose l-arginine and its functional metabolite, l-ornithine, to analyze their effects on food intake in chicks. Intracerebroventricular injection (2μmol) of l-ornithine, but not l-arginine, significantly inhibited food intake in neonatal chicks. In Experiment 3, we found that central injection of l-ornithine (2, 4, and 6μmol) dose-dependently suppressed food intake in chicks. These results suggested that l-ornithine may have an important role in the control of food intake as an acute satiety signal in the neonatal chick brain.

Neuropeptide Y-induced feeding is dependent on GABAA receptors in neonatal chicks

In mammals and birds, neuropeptide Y (NPY) and gamma-aminobutyric acid (GABA) are found in brain areas known to be involved in the control of ingestive behavior and act to increase voluntary food intake. In rats, significant evidence suggest a functional and behavioral interaction between NPY and GABA mediated transmission in various brain regions, including the arcuate and paraventricular nuclei of the hypothalamus which can be important in the regulation of feeding behavior. In the present study, the effect of intracerebroventricular (ICV) administration of NPY and GABA receptor antagonists on food intake was examined in neonatal chicks. The ICV injection of NPY strongly stimulated food intake while co-administration of NPY and picrotoxin, a GABA(A) antagonist, (but not CGP54626, a GABA(B) antagonist) weakened food intake induced by NPY. These results suggest that central NPY stimulates food intake in neonatal chicks by interaction with the GABAergic system via GABA(A) receptors.

The role of GABAergic system on the inhibitory effect of ghrelin on food intake in neonatal chicks

Ghrelin is a gut-brain peptide that has a stimulatory effect on food intake in mammals. In contrast, this peptide decreases food intake in neonatal chicks when injected intracerebroventricularly (ICV). In mammals, neuropeptide Y (NPY) mediates the orexigenic effect of ghrelin whereas in chicks it appears that corticotrophin releasing factor (CRF) is partially involved in the inhibitory effect of ghrelin on food intake. Gamma aminobutyric acid (GABA) has a stimulatory effect on food intake in mammals and birds. In this study we investigated whether the anorectic effect of ghrelin is mediated by the GABAergic system. In Experiment 1, 3h-fasted chicks were given an ICV injection of chicken ghrelin and picrotoxin, a GABAA receptors antagonist. Picrotoxin decreased food intake compared to the control chicks indicating a stimulatory effect of GABAA receptors on food intake. However, picrotoxin did not alter the inhibitory effect of ghrelin on food intake. In Experiment 2, THIP hydrochloride, a GABAA receptor agonist, was used in place of picrotoxin. THIP hydrochloride appeared to partially attenuate the decrease in food intake induced by ghrelin at 30min postinjection. In Experiment 3, the effect of ICV injection of chicken ghrelin on gene expression of glutamate decarboxylase (GAD)1 and GAD2, GABA synthesis enzymes in the brain stem including hypothalamus, was investigated. The ICV injection of chicken ghrelin significantly reduced GAD2 gene expression. These findings suggest that ghrelin may decrease food intake in neonatal chicks by reducing GABA synthesis and thereby GABA release within brain feeding centers.

The role of central CB2 cannabinoid receptors on food intake in neonatal chicks

The endocannabinoids (ECBs) have diverse physiological functions including the regulation of food intake and metabolism. In mammals, ECBs regulate feeding primarily through the CB1 receptors within the brain whereas the CB2 receptors are primarily involved in the regulation of immune function by direct action on peripheral immune cells and central glia. The central effect of ECBs on feeding behavior has not been studied in non-mammalian species. Therefore, the present study investigated the effect of CB65, a selective CB2 receptors agonist, on food intake in the neonatal chicks. In addition, the effect of astressin, a CRF receptor antagonist, on CB65-induced food intake was also investigated. Intracerebroventricular injection of the CB65 (1.25μg) increased the food intake at 30- and 60-min post-injection significantly as compared to the control group. Pretreatment with a selective CB2 receptor antagonist, AM630, but not astressin, significantly attenuated the CB65-induced food intake. These results suggested that CB2 receptor agonists act on the brain to induce food intake.

Intracerebroventricular Administration of Growth Hormone Releasing Peptide-6 (GHRP-6) Inhibits Food Intake, but not Food Retention of Crop and Stomach in Neonatal Chicks

Growth hormone secretagogues (GHS), including ghrelin, are known to stimulate feeding behavior in mammals. In contrast, intracerebroventricular (ICV) injection of rat or chicken ghrelin, strongly inhibits food intake in chicks. The difference prompted us to compare the effect of growth hormone releasing peptide-6 (GHRP-6), one of synthetic GHSs on feeding behavior of chicks with that of ghrelin. Gastric motility stimulating action of GHRP-6 was also examined in vivo measuring retention of food in digestive tracts. ICV injection of GHRP-6 (0.38nmol-1.5nmol) dose-dependently inhibited food intake of neonatal chicks under both ad libitum and fasting conditions. The anorexic effect of GHRP-6 was attenuated by D-Lys3-GHRP-6 (GHS receptor antagonist) in a dose dependent manner. Central injection of GHS agonist and/or antagonist did not affect food retention in crop, proventriculus and gizzard. These results suggest that central injection of synthetic GHS, GHRP-6 inhibits feeding behavior as dose ghrelin without affecting gastrointestinal motility in layer chicks.

Inhibitory effect of ghrelin on food intake is mediated by the corticotropin-releasing factor system in neonatal chicks

It is known that, in rats, central and peripheral ghrelin increases food intake mainly through activation of neuropeptide Y (NPY) neurons. In contrast, intracerebroventricular (ICV) injection of ghrelin inhibits food intake in neonatal chicks. We examined the mechanism governing this inhibitory effect in chicks. The ICV injection of ghrelin or corticotropin-releasing factor (CRF), which also inhibits feeding and causes hyperactivity in chicks. Thus, we examined the interaction of ghrelin with CRF and the hypothalamo-pituitary–adrenal (HPA) axis. The ICV injection of ghrelin increased plasma corticosterone levels in a dose-dependent or a time-dependent manner. Co-injection of a CRF receptor antagonist, astressin, attenuated ghrelin-induced plasma corticosterone increase and anorexia. In addition, we also investigated the effect of ghrelin on NPY-induced food intake and on expression of hypothalamic NPY mRNA. Co-injection of ghrelin with NPY inhibited NPY-induced increase in food intake, and the ICV injection of ghrelin did not change NPY mRNA expression. These results indicate that central ghrelin does not interact with NPY as seen in rodents, but instead inhibits food intake by interacting with the endogenous CRF and its receptor.

Central administration of leucine, but not isoleucine and valine, stimulates feeding behavior in neonatal chicks

Branched-chain amino acids (BCAAs) are essential amino acids that play a major role in brain energy metabolism. This study was done to elucidate whether central injection of BCAAs influences feeding behavior in chicks. We found that the intracerebroventricular injection of leucine (200 μg) significantly stimulated food intake in neonatal chicks during 30 min postinjection. Additionally, the starting time of feeding and pecking rhythm after injection were significantly accelerated by leucine. In contrast, isoleucine and valine had no effect on ingestive response during experiment periods. Moreover, a metabolite of leucine (α-ketoisocaproic acid) at an equimolar concentration of leucine also did not increase food intake in chicks. These results suggest that leucine induces hyperphagia of neonatal chicks and it may be due to the synthesized glutamate by exogenous leucine.

Intracerebroventricular injection of muscimol, baclofen or nipecotic acid stimulates food intake in layer-type, but not meat-type, chicks

This study was designed to compare the effects of muscimol (GABA A agonist), baclofen (GABA B agonist) and nipecotic acid (GABA uptake inhibitor) on food intake in two chicken strains (meat-type and layer-type chicks). The intracerebroventricular (ICV) injection of all GABA agents induced hyperphagia in layer-type chicks. However, in broiler chicks, there were similar tendencies with muscimol and nipecotic acid but not significantly different. Conversely, ICV injection of baclofen depressed feeding of broiler chicks. These results suggest that there are some differences in central GABAergic systems between these strains of chicks, but GABAergic systems have an important role in the regulation of food intake in neonatal chicks.

Chicken ghrelin and growth hormone-releasing peptide-2 inhibit food intake of neonatal chicks

Ghrelin is an endogenous ligand for the growth hormone secretagogue (GHS) receptor. Ghrelin stimulates feeding in rats, however, intracerebroventricular (i.c.v.) injection of rat ghrelin inhibits feeding of neonatal chicks. In the present study, the effect of i.c.v. injection of different ghrelins including chicken and bullfrog ghrelin, and synthetic GH-releasing peptide (GHRP) on feeding of neonatal chicks was investigated. Chicken ghrelin strongly suppressed feeding. To compare the inhibitory effect, chicken and rat ghrelin were examined. The suppressive effect of feeding by chicken and rat ghrelin was almost identical. Bullfrog ghrelin contains a change in the acylated amino acid from Ser to Thr, strongly suppressed feeding. The i.c.v. injection of GHRP-2 (KP-102), a synthetic GHS, also inhibited feeding. These results indicate that the chicken GHS receptor is affected by several forms of GHS, and that food intake of neonatal chicks is inhibited by GHS receptor agonists.

Intracerebroventricular administration of octopamine stimulates food intake of chicks through α 2-adorenoceptor

Octopamine, known to be an important neurotransmitter in invertebrates, has been noted to have several similarities to noradrenaline (NA) in mammals. The present study was done to elucidate whether central injection of octopamine enhances the feeding behavior of chicks and to investigate the interaction of octopamine with both α 1- and α 2-adorenoceptors. We found that the intracerebroventricular injection of octopamine significantly stimulated food intake of neonatal chicks during 30 min postinjection, but not thereafter. Moreover, this octopamine-induced eating response was attenuated by the α 2-antagonist yohimbine, but not by the α 1-antagonist prazosin. These results suggest that the action of octopamine on the feeding behavior of the neonatal chick is similar to that of NA, since octopamine regulates food intake through the α 2-adorenoceptor.

Suppression of food intake induced by corticotropin-releasing factor family in neonatal chicks

Corticotropin-releasing factor (CRF), urocortin and urotensin I share amino acid sequences, and they inhibit food intake in mammals. CRF plays a potent role in decreasing food intake in avian species, but the effects of urocortin and urotensin I have not been investigated. Therefore, the effect of these three peptides on food intake in the neonatal chick was compared. In Experiment 1, birds were injected intracerebroventricularly (i.c.v.) with either 0, 0.01, 0.1 or 1 μg of urocortin following a 3-h fast, and food intake was measured for 2 h post-injection. Food intake was suppressed in a dose-dependent manner. Using a similar design in Experiment 2, the effect of urotensin I was investigated. Urotensin I appeared to suppress food intake in neonatal chicks more than urocortin did. In Experiment 3, the efficacy of CRF, urocortin and urotensin I was directly compared using one dose, 0.1 μg. The results indicated that the suppressive effect on food intake was strongest for CRF followed by urotensin I, then urocortin. These results suggest that the structure of receptors for the CRF family in chicks may be somewhat different than in mammals.

Feeding responses to several neuropeptide Y receptor agonists in the neonatal chick

Neuropeptide Y is one of the most potent neuropeptides known to induce feeding in animals, and has been suggested to be a physiological signal for food intake. It has been also reported that intracerebroventricular injection of neuropeptide Y stimulates feeding behavior of the neonatal chick. There are many neuropeptide Y receptor agonists that have not been investigated in feeding response of the neonatal chick. The aim of this study is to elucidate whether central injection of several neuropeptide Y receptor agonists stimulates feeding of the neonatal chick over 2 h. We found that central injections of [Leu 31, Pro 34]neuropeptide Y, peptide YY, human pancreatic polypeptide and rat pancreatic polypeptide significantly stimulated food intake of neonatal chicks throughout the 2-h post-injection period. Neuropeptide Y-(13–36) significantly stimulated feeding at 30 min, but not thereafter. [ d-Trp 32]neuropeptide Y stimulated feeding at 60 and 120 min, but not 30 min, post-injection. Central administration of rat pancreatic polypeptide, which does not increase food intake in rats, stimulated feeding in chicks. This result reflects structural differences of the neuropeptide Y receptor subtypes and/or differences in mechanisms stimulating feeding behavior between mammals and chickens. In conclusion, neuropeptide Y receptor agonists, except for neuropeptide Y-(13–36), are potent stimulators of food intake in the neonatal chick.