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.

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.

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.

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.

A transdiagnostic systematic review and meta-analysis of ketamine's anxiolytic effects.

BACKGROUND: Ketamine may be effective in treating symptoms of anxiety, but the time profile of ketamine's anxiolytic effect is ill-defined. This systematic review and meta-analysis investigated the anxiolytic effect of ketamine at different time points across a range of clinical settings. METHODS: Electronic databases were searched to capture randomised control trials measuring the anxiolytic effects of ketamine in contexts including mood disorders, anxiety disorders and chronic pain. Meta-analyses were conducted using a random-effects model. The correlations between (1) improvements in mean anxiety and depression scores, and (2) peak dissociation and improvements in mean anxiety scores were also assessed. RESULTS: In all, 14 studies met inclusion criteria. Risk of bias was high in 11 studies. Ketamine significantly reduced anxiety scores compared to placebo at acute (<12 h; standard mean difference (SMD): -1.17, 95% confidence interval (CI) [-1.89, -0.44], p < 0.01), subacute (24 h; SMD: -0.44, 95% CI [-0.65, -0.22], p < 0.01) and sustained (7-14 days; SMD: -0.40, 95% CI [-0.63, -0.17], p < 0.01) time points. Exploratory analyses revealed improvements in anxiety and depression symptoms correlated at both subacute (R2 = 0.621, p = 0.035) and sustained time points (R2 = 0.773, p = 0.021). The relationship between peak dissociation and improvement in anxiety was not significant. CONCLUSIONS: Ketamine appears to offer rapid and sustained anxiety symptom relief across a range of clinical settings, with anxiolytic effects occurring within the first 12 h of administration and remaining effective for 1-2 weeks. Future studies could explore the effects of ketamine maintenance therapy on anxiety symptoms.

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.