Role of the intracerebroventricular injection of the visfatin and its interaction with neuropeptide Y and nitric systems on food intake in neonatal chicken.

Visfatin play an essential role in the central regulation of appetite in birds. This study aimed to determine role of intracerebroventricular (ICV) injection of the visfatin on food intake and its possible interaction with neuropeptide Y (NPY) and nitric oxide system in neonatal broiler chicken. In experiment 1, neonatal chicken received ICV injection visfatin (1, 2 and 4 µg). In experiment 2, chicken received ICV injection of B5063 (NPY1 receptor antagonist 1.25 µg), visfatin (4 µg) and co-injection of the B5063 + Visfatin. In experiments 3-6, SF22 (NPY2 receptor antagonist 1.25 µg), SML0891 (NPY5 receptor antagonist 1.25 µg), L-NAME (nitric oxide synthase inhibitor, 100 nmol) and L-arginine (Precursor of nitric oxide, 200 nmol) were injected instead of B5063. Then the amount of cumulative food was measured at 30, 60 and 120 min after injection. Obtained data showed, injection visfatin (2 and 4 µg) increased food intake compared to control group (P < 0.05). Co-injection of the B5063 + Visfatin decreased visfatin-induced hyperphagia compared to control group (P < 0.05). Co-injection of the L-NAME + Visfatin amplified visfatin-induced hyperphagia compared to control group (P < 0.05). The result showed that visfatin has hyperphagic role and this effect mediates via NPY1 and nitric oxide system in neonatal chicken.

Effects of in ovo injection of the L-carnosine on physiological indexes of neonatal broiler chicken.

The objective of the present investigation was to ascertain the impact of in ovo administration of L-carnosine on physiological indicators in neonatal broiler chickens. A total of 280 viable broiler eggs were allocated to 7 distinct groups: control, Sham in ovo injection of sterile water on d 7 of incubation. Groups 3 and 4 were subjected to in ovo injections of L-carnosine (25 and 50 µg) on d 7 of incubation. Group 5, functioning as a sham in ovo, received an injection of sterile water on d 18 of incubation. Groups 6 and 7 were in ovo injected with L-carnosine (25 and 50 µg) on d 18 of incubation. All eggs were subjected to incubation, and the hatching rate and body weight were measured post-hatch. Subsequently, blood samples were collected, and the levels of biochemical constituents in the serum were determined. Based on the outcomes, the administration of L-carnosine (50 µg) on d 7 of incubation led to a significant increase in post-hatch body weight compared to the control group (P < 0.05). The in ovo injection of L-carnosine (25 and 50 µg) on d 7 and 18 of incubation resulted in a significant decrease in the levels of serum glucose, triglyceride (TG), low-density lipoprotein (LDL), phosphorus (P), alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine transaminase (ALT) in the newly hatched chickens (P < 0.05). Furthermore, the in-ovo injection of L-carnosine (25 and 50 µg) on d 7 and 18 of incubation led to a significant increase in the levels of serum high-density lipoprotein (HDL), calcium, and total protein (TP) in the newly hatched chickens (P < 0.05). Nonetheless, L-carnosine did not have a significant effect on the levels of serum IgY and IgA in the newly hatched chickens (P > 0.05). These findings indicate that the in ovo administration of L-carnosine yielded favorable outcomes in neonatal broiler chickens.

The role of central neurotransmitters in appetite regulation of broilers and layers: similarities and differences.

The importance of feeding as a vital physiological function, on the one hand, and the spread of complications induced by its disorder in humans and animals, on the other hand, have led to extensive research on its regulatory factors. Unfortunately, despite many studies focused on appetite, only limited experiments have been conducted on avian, and our knowledge of this species is scant. Considering this, the purpose of this review article is to examine the role of central neurotransmitters in regulating food consumption in broilers and layers and highlight the similarities and differences between these two strains. The methodology of this review study includes a comprehensive search of relevant literature on the topic using appropriate keywords in reliable electronic databases. Based on the findings, the central effect of most neurotransmitters on the feeding of broilers and laying chickens was similar, but in some cases, such as dopamine, ghrelin, nitric oxide, and agouti-related peptide, differences were observed. Also, the lack of conducting a study on the role of some neurotransmitters in one of the bird strains made it impossible to make an exact comparison. Finally, it seems that although there are general similarities in appetite regulatory mechanisms in meat and egg-type chickens, the long-term genetic selection appropriate to breeding goals (meat or egg production) has caused differences in the effect of some neurotransmitters. Undoubtedly, conducting future studies while completing the missing links can lead to a comprehensive understanding of this process and its manipulation according to the breeding purposes of chickens.

Central effects of the serotoninergic, GABAergic, and cholecystokinin systems on neuropeptide VF (NPVF)-induced hypophagia and feeding behavior in neonatal broiler chicken.

The study was performed to evaluate the role of central serotoninergic, GABAergic, and cholecystokinin systems in neuropeptide VF (NPVF)-induced hypophagia in broiler chickens. In this study, 9 experiments were designed, each with one control and three treatment groups (n = 44 in each experiment). Control chicks of all groups were subjected to normal saline + Evans blue 0.1 % Intracerebroventricular (ICV) injection. In the first experiment, 3 groups of chicks received NPVF (4, 8, and 16 nmol). In experiment 2-9, one group of chicks received NPVF (16 nmol), another received 10 µg fluoxetine (serotonin reuptake inhibitor) (experiment 2), 1.25 µg PCPA (serotonin synthesis inhibitor) (experiment 3), 1.5 µg SB-242,084 (5-HT2C receptor antagonist) (experiment 4), 15.25 nmol 8-OH-DPAT (5-HT1A receptor antagonist) (experiment 5), 0.5 µg picrotoxin (GABAA receptor antagonist) (experiment 6), 20 ng CGP54626 (GABAB receptor antagonist) (experiment 7), 1 nmol devazepide (CCKA receptor antagonist) (experiment 8), and 1 nmol/L-365(-|-),260 (CCKB receptor antagonist) (experiment 9), and another final group received combination of specific neurotransmitter + NPVF Then, the cumulative food intake was measured until 120 min post-injection. ICV injection of NPVF (8 and 16 nmol) significantly decreased food intake (P < 0.05). Simultaneous injection of fluoxetine + NPVF and also picrotoxin + NPVF significantly increased hypophagia caused by NPVF (P < 0.05). However, co-administration of PCPA + NPVF and also SB242084 + NPVF significantly decreased NPVF-induced hypophagia (P < 0.05). Finally, 8-OH-DPAT, CGP54626, devazepide, and L-365,260 had no effect on the hypophagia brought on by NPVF (P > 0.05). Count-type behaviors were dose-dependent and decreased in groups that received NPVF compared to the control group (P < 0.05). Our finding recommended an interconnection between central NPVF and serotoninergic, GABAergic, and cholecystokinin systems in neonatal chickens.

The effects of neuropeptide W on food consumption and feeding behavior in neonatal meat-type chicks: Role of CRF1/CRF2 and NPY1 receptors.

In several studies, the regulatory role of the neuropeptide W (NPW) system in food intake has been demonstrated. Considering the lack of avian studies in this field, the current research was conducted to evaluate the effects of intracerebroventricular (ICV) infusion of NPW and its interferences with corticotropin, melanocortin, and neuropeptide Y (NPY) receptors on meal consumption and feeding behaviors of broilers. In the first experiment, birds were injected with NPW (0.75, 1.5, and 3 nmol) in addition to saline. In the second experiment, saline, CRF1 receptor antagonist (NBI35965, 30 µg), NPW (3 nmol), and simultaneous injections of NBI35965 and NPW were performed. Experiments 3-8 were identical to experiment 2, except that CRF2 receptor antagonist (K41498, 30 µg), MC3/MC4 receptor antagonist (SHU9119, 0.5 nmol), MC4 receptor antagonist (HS024, 0.5 nmol), NPY1 receptor antagonist (BMS193885, 1.25 nmol), NPY2 receptor antagonist (CYM9484, 1.25 nmol), and NPY5 receptor (antagonist L-152,804, 1.25 nmol) were administrated instead of NBI35965. After that, cumulative feed intake and feeding behavior were monitored for 2 h and 30 min after injections, respectively. Following the infusion of NPW (1.5 and 3 nmol), there was a significant stimulation of meal consumption in chickens (P < 0.05). Concomitant injection of NBI35965 and K41498 with NPW enhanced the appetite-increasing effect of NPW (P < 0.05); while BMS193885 suppressed this effect of NPW (P < 0.05). Injection of SHU9119, HS024, CYM9484, and L-152804 with NPW at the same time, had no significant effect on NPW-induced hyperphagia (P > 0.05). NPW also significantly decreased the standing period and the number of jumps, steps, and exploratory pecks, and led to an increase in sitting period and feeding pecks (P < 0.05). Based on the observations, it seems that NPW-induced hyperphagia could be mediated through CRF1, CRF2, and NPY1 receptors in neonatal broilers.

Resveratrol plays neuroprotective role on ketamine-induced schizophrenia-like behaviors and oxidative damage in mice.

This study aimed to determine effects of the resveratrol on ketamine-induced schizophrenia-like behaviors and oxidative damage in mice. Twenty-four male mice were allocated into four experimental groups as control, ketamine (20 mg/kg), resveratrol (80 mg/kg) and co-administration of the ketamine (20 mg/kg) + resveratrol (80 mg/kg). Mice were received resveratrol for 30 days and ketamine was used for an animal model of schizophrenia and was injected from days 16 to 30 of the study. After the drug administration was finished, schizophrenia-like behaviors were evaluated using object recognition test, tail suspension test, forced swimming test and open field test and brain malondialdehyde, glutathione peroxidase, superoxide dismutase and catalase levels were determined. According to the results, ketamine treatment significantly decreased body weight and pretreatment with resveratrol elevated body weight compared to ketamine group (P < 0.05). Ketamine treatment significantly decreased number of the cross in open field test and pretreatment with resveratrol improved i (P < 0.05). Immobility time in tail suspension and forced swimming tests increased in mice treated with ketamine (P < 0.05). Pretreatment with resveratrol diminished immobility time compared to ketamine group (P < 0.05). Ketamine significantly decreased memory deficits while pretreatment with resveratrol significantly reduced the memory deficits induced by ketamine (P < 0.05). Brain MDA increased in both cortical and sub-cortical area in ketamine treated mice while pretreatment with resveratrol decreased ketamine-induced elevation in MDA (P < 0.05). Ketamine significantly decreased brain SOD, GPx and CAT levels while pretreatment with resveratrol improved SOD, GPx and CAT levels (P < 0.05). Findings suggested resveratrol has neuroprotective effects against ketamine-induced behavioral deficits and oxidative damages.

Maternal music exposure during pregnancy influences reflexive motor behaviors in mice offspring.

Evidence supports that music can modulate many physiological roles, exerting clear effects on the central nervous system. For this effect to be positive, music should be tuned at a frequency of 432 Hz. This study aims to determine the effects of prenatal exposure to music on reflexive motor behaviors in mice offspring. Six pregnant female NMRI mice (8-10 weeks old) were randomly and equally allocated into two groups. Group 1 as control was placed in a normal housing area (average room noise 35 dB), and Group 2 was exposed to music pitched at 432 Hz for 2 h a day played at constant volume (75/80 dB) during pregnancy. Following delivery, four pups from each pregnant mouse were selected, and reflexive motor behaviors including ambulation, hind-limb foot angle, surface righting, grip strength, front- and hind-limb suspension, and negative geotaxis were determined. Based on the findings, prenatal exposure to music significantly increased ambulation score, grip strength, and front- and hind-limb suspension compared to the control group (P < 0.05). Also, prenatal exposure to music significantly decreased hind-limb foot angle, negative geotaxis, and surface righting compared to the control group (P < 0.05). These results suggested that music exposure during pregnancy had a significant positive effect on all tested reflexive motor behaviors in mice offspring.

Hypophagia induced by intracerebroventricular injection of apelin-13 is mediated via CRF1/CRF2 and MC3/MC4 receptors in neonatal broiler chicken.

Previous studies have shown the role of apelin and its receptors in the regulation of food intake. In the present study, we investigate the mediating role of melanocortin, corticotropin, and neuropeptide Y systems in apelin-13- induced food intake in broilers. Eight trials were run in the current investigation to ascertain the relationships between the aforementioned systems and apelin-13 on food intake and behavioral changes after apelin-13 administration. In experiment 1, hens were given an intracerebroventricular administration of a solution for control in addition to apelin-13 (0.25, 0.5, and 1 µg). Astressin-B (a CRF1/CRF2 receptor antagonist, 30 µg), apelin-13 (1 µg), and administration of astressin-B and apelin-13 concurrently, were all injected into the birds in experiment 2. Experiments 3 through 8 were quite similar to experiment 2, with the exception of astressin2-B (CRF2 receptor antagonist, 30 µg), SHU9119 (MC3/MC4 receptor antagonist, 0.5 nmol), MCL0020 (MC4 receptor antagonist, 0.5 nmol), BIBP-3226 (NPY1 receptor antagonist, 1.25 nmol), BIIE 0246 (NPY2 receptor antagonist, 1.25 nmol), and CGP71683A (NPY5 receptor antagonist, 1.25 nmol) were injected instead of astressin-B. After then, total food consumption was monitored for 6 h. Apelin-13 injections of 0.5 and 1 µg decreased feeding (P < 0.05). The hypophagic effects of apelin were attenuated following the simultaneous administration of Astressin-B and Astressin2-B with apelin-13 (P > 0.05). Co-infusion of SHU9119 and apelin-13 reduced the appetite-decreasing effects of apelin-13 (P > 0.05). When MCL0020 and apelin-13 were injected at the same time, the hypophagia that apelin-13 induced was eliminated (P > 0.05). BIBP-3226, BIIE 0246, and CGP71683A had no effect on the hypophagia brought on by apelin-13 (P > 0.05). Also, apelin-13 significantly increased number of steps, jumps, exploratory food, pecks and standing time while decreased siting time (P < 0.05). These findings suggest that apelin-13-induced hypophagia in hens may involve the CRF1/CRF2 and MC3/MC4 receptors.

Restraint stress potentiates sensitivity to the antinociceptive effect of morphine through orexin receptors in the ventral tegmental area.

Orexin signaling in the ventral tegmental area (VTA) plays a critical role in stress and addictive behaviors. On the other hand, exposure to stress potentiates behavioral sensitization to drugs of abuse such as morphine. This study aimed to elucidate the role of orexin receptors within the VTA in restraint stress (RS)-induced morphine sensitization. Adult male albino Wistar rats underwent stereotaxic surgery, and two stainless steel guide cannulae were bilaterally implanted into the VTA. Different doses of SB334867 or TCS OX2 29 as orexin-1 (OX1) and orexin-2 (OX2) receptor antagonists were microinjected into the VTA five min before exposure to RS, respectively. A duration of three hours was considered for applying the RS, and 10 min after RS exposure, animals received a subcutaneous injection of an ineffective dose of morphine (1 mg/kg) for three consecutive days followed by a five-day drug/stress-free period. On the ninth day, the tail-flick test evaluated the sensitivity to the antinociceptive effects of morphine. The results demonstrated that the sole application of RS or morphine (1 mg/kg) could not induce morphine sensitization; however, concurrent application of RS and morphine could induce morphine sensitization. Besides, intra-VTA administration of OX1 R or OX2 R antagonists before paired administration of morphine and RS blocked morphine sensitization. The role of OX1 R and OX2 R in the induction of stress-induced morphine sensitization was almost identical. This study provides new insight into the role of orexin signaling in the VTA in the potentiation of morphine sensitization induced by RS and morphine co-administration.

Role of central adiponectin and its interactions with NPY and GABAergic systems on food intake in neonatal layer chicken.

BACKGROUND & AIM: Adiponectin is a member of the adipokine family and contributes to regulating energy homeostasis, reproduction, and various biological functions, such as insulin receptor signaling pathway sensitivity, mitochondrial biogenesis, oxidative metabolism, neurogenesis, and suppression of inflammation. This study aimed to investigate the effects of intracerebroventricular (ICV) injection of adiponectin and its interaction with the neuropeptide Y (NPY) and GABAergic systems on central appetite regulation in neonatal layer-type chickens. MATERIALS & METHODS: In this study, 6 experiments were conducted, each of which included 4 experimental groups. In the first experiment, the chickens were injected with saline and adiponectin (20.73, 41.45, and 62.18 nmol). In the second experiment, saline, adiponectin (62.18 nmol), B5063 (NPY1 receptor antagonist, 2.12 nmol), and simultaneous injections of adiponectin and B5063 were performed. Experiments 3 to 6 were done in the same way to experiment 1, but the chickens were injected with SF22 (NPY2 receptor antagonist, 2.66 nmol), SML0891 (NPY5 receptor antagonist, 2.89 nmol), picrotoxin (GABAA receptor antagonist, 0.89 nmol), CGP54626 (GABAB receptor antagonist, 0.047 nmol) instead of B5063. Feed consumption was measured 120 min after the injection. RESULTS: A dose-dependent increase in appetite was observed after the injection of adiponectin (20.73, 41.45, and 62.18 nmol) (P < 0.05). The injection of B5063 + adiponectin attenuated the hyperphagic effect of adiponectin (P < 0.05). In addition, co-injection of picrotoxin and adiponectin significantly decreased adiponectin-induced hyperphagia (P < 0.05). In addition, adiponectin significantly increased the number of steps, jumps, exploratory food, pecks, and standing time, while decreasing sitting time and rest time (P < 0.05). CONCLUSION: These results suggest that the hyperphagic effects of adiponectin are probably mediated through NPY1 and GABAA receptors in neonatal layer-type chickens.

Central effects of opioidergic system on food intake in birds and mammals: a review.

Undoubtedly, the food intake process is one of the most necessary physiological functions for the survival of animals and humans. Although; this operation seems simple on the surface, the regulation of the mechanisms involved in it requires the cooperation of many neurotransmitters, peptides, and hormonal factors in the nervous and endocrine systems. Understanding the signals that regulate energy levels and appetite, may open new approaches to therapeutics and drugs used in obesity-related complications. Improving the quality of animal products and health is also possible due to this research. The present review is aimed to sum up the current findings on central effects of opioids on the food consumption of birds and mammals. Based on the reviewed articles, the opioidergic system appears to be one of the key elements in the birds' and mammals' food intake and is closely related to other systems involved in appetite regulation. According to the findings, it seems that the effects of this system on nutritional mechanisms are often applied via kappa- and mu-opioid receptors. Controversial observations have been made regarding opioid receptors, highlighting the need for further studies, especially at the molecular level. The role of opiates in taste or diet craving also showed the efficacy of this system, especially the mu-opioid receptor, on preferences such as diets containing high sugar and fat. Finally, putting the results of this study together with the findings of human experiments and other primates can lead to a correct comprehension of the appetite regulation processes, especially the role of the opioidergic system.

Effect of troxerutin consumption during gestation period on reflexive motor behavior in mice offspring.

This study aimed to determine the effects of troxerutin consumption during gestation on reflexive motor behavior in mice offspring. Forty pregnant female mice were allocated into four groups. In the control group, mice received water, while in groups 2-4, female mice p.o. administered troxerutin (50, 100, and 150 mg/kg) at 5, 8, 11, 14, and 17 days of gestation (GD). Following delivery, pups were selected based on their experimental group, and reflexive motor behaviors were determined. Also, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant status (TAS) were determined. Based on the findings, maternal exposure to troxerutin (100 and 150 mg/kg) increased ambulation scores in offspring's compared with control group (P < 0.05). Also, prenatal exposure to troxerutin increased front- and hind-limb suspension scores in newborns compared with control group (P < 0.05). Maternal exposure to troxerutin increased grip strength and negative geotaxis in newborns in comparison with control mice (P < 0.05). Prenatal exposure to troxerutin (100 and 150 mg/kg) decreased hind-limb foot angle and surface righting in pups compared with control group (P < 0.05). Maternal exposure to troxerutin decreased MDA production and increased SOD, GPx, and TAS levels in offspring (P < 0.05). These results suggested that prenatal consumption of the troxerutin improves reflexive motor behaviors in mice pups.

Relationship between obesity-related markers, biochemical metabolic parameters, hormonal profiles and sperm parameters among men attending an infertility clinic.

Obesity causes many health problems as well as has negative effects on fertility. However, little is known about the association between obesity-related markers (hip circumference (HC), waist circumference (WC), waist to hip ratio (WHR), waist to height ratio (WHtR), body fat mass (BFM), skeletal muscle (SM), resting metabolism (RM), visceral fat (VF), and visceral adiposity index (VAI)) and sperm parameters. This cross-sectional study was conducted on 98 men in three groups: normal-weight (Nw; body mass index: BMI < 25 kg/m2 ), overweight (Ow; BMI: 25-29 kg/m2 ), and obese (Ob; BMI: 30-35 kg/m2 ) to investigate this issue. The mean WC, HC, WHtR, BFM, SM, RM, and VF were remarkably higher (p < 0.001) for subjects in the Ob group than in Ow and Nw. In Nw, positive correlations were observed between BFM (r = 0.402) and VAI (r = 0.353) and sperm progressive motility (p < 0.05). In Ob males, there was a positive correlation (r = 0.430) between sperm progressive motility and height and a negative relation (r = -0.447) between sperm progressive motility and WHtR. We found the association between serum testosterone (T) levels, T/estradiol ratios, and semen parameters being dependent on obesity-related markers which confirms the negative effects of obesity on male hormones. In conclusion, WHtR is a valuable parameter in infertility clinics that warrants further studies.

Molecular mechanisms highlighting the potential role of COVID-19 in the development of neurodegenerative diseases.

Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In addition to the pulmonary manifestations, COVID-19 patients may present a wide range of neurological disorders as extrapulmonary presentations. In this view, several studies have recently documented the worsening of neurological symptoms within COVID-19 morbidity in patients previously diagnosed with neurodegenerative diseases (NDs). Moreover, several cases have also been reported in which the patients presented parkinsonian features after initial COVID-19 symptoms. These data raise a major concern about the possibility of communication between SARS-CoV-2 infection and the initiation and/or worsening of NDs. In this review, we have collected compelling evidence suggesting SARS-CoV-2, as an environmental factor, may be capable of developing NDs. In this respect, the possible links between SARS-CoV-2 infection and molecular pathways related to most NDs and the pathophysiological mechanisms of the NDs such as Alzheimer's disease, vascular dementia, frontotemporal dementia, Parkinson's disease, and amyotrophic lateral sclerosis will be explained.

Central dopaminergic, serotoninergic, as well as GABAergic systems mediate NMU-induced hypophagia in newborn chicken.

AIM: Dopaminergic, serotoninergic, and GABAergic systems influence feeding; however, it is unknown how these chemicals interact with neuromedin U (NMU)-induced feeding in birds. In the current study, ten trials were conducted to determine the links between the above-mentioned systems and NMU. MATERIALS AND METHODS: In the foremost experimentation, chickens were given intracerebroventricularly injections of NMU (0.1, 1, and 10 µg). NMU (10 µg), SCH23390 (5 nmol), a D1 receptor antagonist, and NMU + SCH23390 were administered in the second experiment. In subsequent experiments, instead of SCH23390, were applied AMI-193 (5 nmol D2 receptor antagonist), NGB2904 (6.4 nmol D3 receptor antagonist), L-741,742 (6 nmol D4 receptor antagonist), 6-OHDA (2.5 nmol dopamine inhibitor), SB242084 (5-HT2c receptor antagonist, 1.5 µg), 8-OH-DPAT (5-HT1A receptor agonist, 15.25 nmol), picrotoxin (GABAA receptor antagonist, 0.5 µg), and CGP54626 (GABAB receptor antagonist, 20 ng). Then, cumulative intake of food was recorded for 2 h. RESULTS: According to the results, NMU reduced feeding when compared to the control group (p < 0.05). The NMU-induced hypophagia was reduced with co-injection of NMU and SCH23390 (p < 0.05). Hypophagia was diminished with NMU and AMI-193 (p < 0.05). NMU + NGB2904 and NMU + L-741,742 co-injections had no influence (p > 0.05). 6-OHDA reduced the hypophagia (p < 0.05). NMU and SB242084 decreased the hypophagia (p < 0.05), whereas NMU and 8-OH-DPAT had no effect (p > 0.05). The effects were amplified with picrotoxin (p < 0.05). NMU with CGP54626 had no influence on the hypophagia (p > 0.05). CONCLUSION: Thus, NMU-induced hypophagia is probably mediated by D1/D2, 5-HT2c, and GABAA receptors in neonatal chicks.

Opioid receptor µ, not δ and κ, modulate food intake induced by ghrelin in laying chickens.

Evidence from animal studies suggests that the opioidergic system and ghrelin have a regulatory role in food intake, but their interaction(s) have not been studied in laying chickens. So in this study, four experiments (each included four groups) were designed. The first experiment was performed to evaluate the effect of ghrelin on the cumulative food intake. Experiments 2-4 were designed to investigate the possibility of µ, δ, or κ opioid receptors mediating ghrelin-induced hypophagia. All drugs were injected intracerebroventricularly (ICV) at 5 days of age. The results of this study showed that the ICV injection of 1.5 nmol ghrelin did not affect cumulative food intake. However, ICV injection of ghrelin with doses of 3 and 6 nmol significantly reduced the cumulative food intake (p < 0.05). However, co-injection of ghrelin with naltrindole and norbinaltorphimine did not show a significant change in decreased food intake compared with ghrelin. Also, opioid µ receptor gene expression significantly increased (p < 0.05), but δ and κ opioid receptors' gene expression did not significantly change. These results indicated that the opioidergic system is involved in developing ghrelin-induced hypophagic effects in laying chickens. Accordingly, this effect of ghrelin to modify the nutritional behavior is possibly mediated by opioid µ receptor.

Possible interaction of central noradrenergic, serotoninergic and oxytocin systems with nesfatin-1 induced hypophagia and feeding behavior in newborn broiler.

There are some differences between mammals and birds in terms of central food intake regulation. In avian species, the hypophagic role of nesfatin-1 has not been investigated with other neurotransmitters. Therefore, this study aimed to determine the alteration of feeding behavior following intracerebroventricular (ICV) injection of nesfatin-1 and its possible interaction with central noradrenergic, serotoninergic, and oxytocin systems in newborn broiler chicks. In experiment 1, birds received ICV injection of phosphate-buffered saline (PBS), prazosin (α1 receptors antagonist, 10 nmol), nesfatin-1 (40 ng), and co-administration of prazosin and nesfatin-1. Experiments 2-10 were similar to experiment 1, except that yohimbine (α2 receptors antagonist, 13 nmol), metoprolol (ß1 receptors antagonist, 24 nmol), IC1118,551 (ß2 receptors antagonist for, 5nmol), SR59230R (ß3 receptors antagonist, 20 nmol), fluoxetine (serotonin reuptake inhibitor, 10 µg), PCPA (serotonin synthesis inhibitor, 1.5 µg), 8-OH-DPAT (5-HT1A receptors agonist, 15.25 nmol), SB242084 (5-HT2C receptors antagonist,1.5 µg) and tocinoic acid (oxytocin receptors antagonist, 2 µg) were injected instead of prazosin. Immediately after the injection, food consumption and behavioral traits were recorded. Nesfatin-1 decreased food consumption (P < 0.05). Nesfatin-1 along with ICI118551 decreased food consumption (P < 0.05). The nesfatin-1- induced hypophagia were reduced by the simultaneous injection of PCPA and nesfatin-1 (P < 0.05). Nesfatin-1induced hypophagia were decreased by the simultaneous injection of SB242084 (P < 0.05). The nesfatin-1 -induced hypophagia were abolished by the simultaneous injection of the tocinoic acid and nesfatin-1 (P < 0.05). ICV injection of the nesfatin-1 decreased the number of steps, jumps, exploratory food, and pecks (P < 0.05) with no effect on drink pecks (P > 0.05). Nesfatin-1 significantly decreased standing time and increased both sitting time and rest time (P < 0.05). Nesfatin-1 could play an important role in feeding behavior, and its hypophagic effects were mediated by ß2 adrenergic, 5-HT2C serotoninergic, and oxytocin receptors in neonatal chickens.

Possible effects of the central adrenergic and dopaminergic receptors on hypophagia induced by neuromedin S in neonatal layer-type chicks.

The current study was aimed to determine the possible effects of the central adrenergic and dopaminergic receptors in neuromedin S (NMS)-induced hypophagia in neonatal layer-type chickens. In the first experiment, control solution, and NMS (0.25, 0.5, and 1 nmol), were injected (intracerebroventricular (ICV)) in chickens. In the second experiment, birds were injected with a control solution,SCH23390 (D1receptor antagonist, 5 nmol), NMS (1 nmol), and a combination of the SCH23390 + NMS. Experiments 3-11 were similar to experiment 2, except that chickens were injected withAMI-193 (D2receptor antagonist, 5 nmol), NGB2904(D3receptor antagonist, 6.4 nmol), L-741,742(D4receptor antagonist, 6 nmol), 6-OHDA(6-hydroxydopamine, 2.5 nmol),Prazosin(α1receptor antagonist, 10 nmol),Yohimbine(α2receptor antagonist, 13 nmol),Metoprolol(ß1receptor antagonist receptor, 24 nmol),ICI 118,551 (ß2receptor antagonist, 5 nmol),SR 59230R (ß3 receptor antagonist, 20 nmol) instead ofSCH23390. Then, cumulative food intake was recorded at 30, 60, and 120 min following the injection. According to the results, food intake was significantly decreased after ICV injection of NMS in a dose -dependent manner (P < 0.05). Also, the co-injection of the SCH23390 + NMS significantly attenuated NMS-induced hypophagia (P < 0.05). The co-administration of AMI-193 + NMS significantly reduced NMS- induced hypophagia (P < 0.05). In addition, the co-injection of ICI 118,551 + NMS and 6-OHDA + NMS considerably decreased NMS-induced food consumption (P < 0.05). However, NGB2904, L-741742, Prazosin, Yohimbine, Metoprolol and SR 59230R had no effect on hypophagia induced by NMS (P > 0.05). These results demonstrated thatNMS- induced hypophagia might be mediated by D1/D2 dopaminergic andß2adrenergic receptors in neonatal layer-type chickens.

Effects of intracerebroventricular injection of spexin and its interaction with NPY, GalR2 and GalR3 receptors on the central food intake regulation and nutritional behavior in broiler chickens.

Food intake and appetite in birds can be adjusted by the complex homeostatic control mechanisms. There seem to be many similarities between mammalian and avian species in terms of the regulatory feeding systems. Therefore, the aim of this study was to investigate the effects of ICV injection of spexin and its interaction with GalR and NPY receptors on central food intake regulation and nutritional behavior in broiler chickens. In experiment 1, chicken received ICV injection of saline, spexin (2.5 nmol), spexin (5 nmol) and spexin (10 nmol). In experiment 2, birds received ICV injection of saline, B5063 (NPY1 receptor antagonist 1.25 µg), spexin (10 nmol) and B5063 + spexin. In experiments 3-6, SF22 (NPY2 receptor antagonist,1.25 µg), ML0891 (NPY5 receptor antagonist,1.25 µg), M871 (GalR2 receptor antagonist,10 nmol) and SNAP37889 (GalR3 receptor antagonist,10 nmol) were injected in chickens instead of B5063. Then food intake was measured until 120 min after the injection and nutritional behavior was monitored at 30 min after the injection. Based on the data, a dose-dependent hypophagia was observed by the injection of spexin (P < 0.05). Concomitant injection of B5063 + spexin enhanced spexin-induced hypophagia (P < 0.05). Co-injection of SNAP37889 + spexin (10 nmol) attenuated -induced hypophagia (P < 0.05). Spexin (5 and 10 nmol) decreased number of steps, jumps, the exploratory food and pecks at 15 min after the injection (P < 0.05). Spexin (5 and 10 nmol) decreased standing time while siting time and rest time increased at 10 min after injection (P < 0.05). Based on observations, spexin-induced hypophagia could be mediated by NPY1 and GalR3 receptors in neonatal broiler chickens.

Role of orexinergic receptors within the ventral tegmental area in the development of morphine sensitization induced by forced swim stress in the rat.

The ventral tegmental area (VTA) has been suggested as part of a common system for reward, stress, and morphine sensitization. Repeated exposure to stress enhances sensitivity to drugs such as morphine. The role of orexin receptor type 1 (OX1R) and type 2 (OX2R) within the VTA in cross-sensitization of morphine with stress was assessed in this study. Various doses of OX1R antagonist (SB334867) and OX2R antagonist (TCS OX2 29) were microinjected into the VTA of 134 adult male albino Wistar rats through cannulae, which had been bilaterally implanted above this region. Five min after microinjection, animals were forced to swim for 6 min, and 10 min after forced swim stress (FSS) termination, a low dose of morphine (i.e., ineffective dose for sensitization) was subcutaneously injected (1 mg/kg; sc). This procedure was repeated for three consecutive days as a sensitization period followed by a 5-day drug/stress-free period. On the 9th day, sensitivity to morphine was examined by measuring antinociceptive responses to the ineffective dose of morphine via tail-flick test. The obtained findings revealed that while concurrent administration of FSS and an ineffective dose of morphine (1 mg/kg; sc) for three consecutive days induced sensitivity to morphine, intra-VTA administration of OX1R- and OX2R antagonists, dose-dependently blocked this sensitization. These results suggested that both orexin receptors located in the VTA have a considerable role in morphine sensitization induced by concurrent administration of FSS and a low dose of morphine. So, there is a contribution of the orexin system partly to stress-induced sensitization to morphine.