Brian C. Prall

Differential Appetite-Related Responses to Central Neuropeptide S in Lines of Chickens Divergently Selected for Low or High Body Weight

The anorexigenic 20 amino acid neuropeptide S (NPS) has not been studied in an animal model of hypo‐ or hyperphagia. The present study aimed to elucidate whether central NPS appetite‐related effects are different in lines of chickens that had undergone long‐term divergent selection for low (LWS) or high (HWS) body weight and that were hypo‐ and hyperphagic, respectively. It took a longer time for food intake to be reduced in LWS than HWS chicks administered the lowest dose of NPS tested (0.14 nmol) and, at the highest dose tested (0.56 nmol), they had a greater reduction in food intake than did HWS chicks. HWS chicks responded with a similar magnitude of food intake reduction that was independent of NPS dose. Although water intake was reduced concurrently with food intake after central NPS in both lines, blood glucose concentrations were not affected. Hypothalamic signalling was different between the lines. Although both lines respond to central NPS with decreased c‐Fos immunoreactivity in the lateral hypothalamus, the periventricular nucleus had increased c‐Fos immunoreactivity in LWS but not HWS chicks. After central NPS treatment, there was increased c‐Fos immunoreactivity in the paraventricular nucleus in HWS but not LWS chicks. These data support the notion of differences in the central NPS system between the LWS and HWS lines and infer that central NPS may differentially affect appetite‐related processes in other species that contain hypo‐ and hyperphagic individuals.

Central visfatin causes orexigenic effects in chicks

Intracerebroventricular injection of visfatin caused increased feed intake and pecking efficiency, but did not affect water intake in chicks. Visfatin-treated chicks had increased c-Fos immunoreactivity in the lateral hypothalamus, decreased reactivity in the ventromedial hypothalamus and the dorsomedial hypothalamus, infundibular nucleus, periventricular nucleus, paraventricular nucleus were not affected. A low dose of visfatin increased locomotion. We conclude that intracerebroventricular injection of visfatin causes orexigenic effects in chicks.

Differential feed intake responses to central corticotrophin releasing factor in lines of chickens divergently selected for low or high body weight.

Effects of intracerebroventricular (ICV) injection of corticotrophin releasing factor (CRF) on feed intake were evaluated in two lines of White Plymouth Rock chickens that have been selected from a common base population for high (HWS) or low (LWS) juvenile body weight. Both lines responded with reduced feed intake after ICV CRF; however, the threshold of response was lower in line LWS than HWS. Additionally, the effects of two receptor antagonists, astressin and alpha-helical CRF (9-41; alpha-CRF), and the effect of CRF fragment 6-33, (which displaces CRF from its binding protein), were evaluated in these lines. Although all three antagonists increased feed intake in line LWS but not line HWS, they attenuated the appetite-reducing effects of CRF only in line HWS. Peripheral plasma corticosterone concentrations after an acute stressor were higher in line LWS than in line HWS. These data support the thesis of correlated responses in the CRF system to selection for high or low juvenile body weight. These differences may contribute to differential feed intake, and hence altered body weights.

The threshold of insulin-induced hypophagia is lower in chicks selected for low rather than high juvenile body weight

Chicks genetically selected for low juvenile body weight had a lower threshold of central insulin-induced decreased food and water intake and whole blood glucose concentration than those selected for juvenile high body weight. Plasma corticosterone concentration was increased but not differently between lines. Therefore, selection may have affected insulin sensitivity which may have then contributed to their hypo- and hyperphagia and differential body weights.

The threshold of amylin-induced anorexia is lower in chicks selected for low compared to high juvenile body weight.

Chicks that have undergone long-term selection for low body weight responded to intracerebroventricular amylin injection with reduced food intake at a dose considerably lower and with a greater magnitude suppression than those selected for high body weight. Behaviors unrelated to ingestion were not affected. These data support the thesis of correlated amylin system responses to selection for low or high body weight, with possible implications to other species.

Satiety induced by central stresscopin is mediated by corticotrophin-releasing factor receptors and hypothalamic changes in chicks.

The central mechanism that mediates stresscopin (SCP)-induced satiety is poorly understood, and its effect on avian appetite is not documented. Thus, this study was conducted to elucidate some of the central and behavioral mechanisms that are associated with SCP-induced satiety using broiler- and layer-type chicks (Gallus gallus) as model organisms. In Experiment 1, broiler-type chicks responded with decreased food and water intake but had increased plasma corticosterone concentration after intracerebroventricular (ICV) SCP injection. However, the effect on water intake was secondary to food intake, since food-restricted SCP-treated broiler-type chicks did not reduce water intake in Experiment 2. In Experiment 3, layer-type chicks responded with decreased food intake at much lower doses than broiler-type chicks. In Experiment 4, astressin (a non-selective corticotrophin-releasing factor [CRF] receptor antagonist) prevented SCP-induced anorexia in broiler-type chicks. In Experiment 5, SCP-treated broiler-type chicks had an increased number of c-Fos immunoreactive cells in the ventromedial hypothalamus, parvicelluar and magnocellular divisions of the paraventricular nucleus and the periventricular nucleus. In Experiment 6, SCP-treated broiler-type chicks had decreased feeding pecks and increased jumping, distance moved and more escape attempts. Thus, we conclude that central SCP causes anorexigenic and other behavioral effects in chicks, and the hypothalamus and CRF receptors are involved.

β‐Melanocyte‐Stimulating Hormone Potently Reduces Appetite Via the Hypothalamus in Chicks

The melanocortin system together with other appetite‐related systems plays a significant role in appetite regulation. The appetite‐related effects of one such melanocortin, β‐melanocyte‐stimulating hormone (MSH), are well documented in rodents; however, its effects in the avian class are not thoroughly understood. Thus, we designed a study to determine the effects of i.c.v. β‐MSH injection on food and water intake, plasma corticosterone concentration, ingestive and non‐ingestive behaviours, and hypothalamic neuronal activation using Cobb‐500 chicks. Chicks responded to β‐MSH‐treatment with a reduction in food and water intake; however when water intake was measured independently of food intake, it was not affected. β‐MSH‐treated chicks also had increased plasma corticosterone concentrations and increased c‐Fos reactivity in the periventricular, paraventricular and infundibular nuclei, and the ventromedial hypothalamus; however, the lateral hypothalamus was not affected. The effect on food intake is primary because behaviours that may be competitive with food intake were not increased in β‐MSH‐treated chicks. Based on these results, we conclude that β‐MSH causes anorexigenic effects that are likely primarily mediated via stimulation of satiety‐related hypothalamic nuclei in broiler‐type chicks.

Central and peripheral alytesin cause short-term anorexigenic effects in neonatal chicks

We studied the effects of alytesin, a natural analogue of bombesin, on appetite-related responses and behaviors in neonatal chicks. Chicks responded to both intracerebroventricular (ICV) and peripheral injections of alytesin with short-term reduced feed intake. ICV alytesin caused reduced short-term water intake when feed was present, but we determined this effect was secondary to feed intake since an effect on water intake was not detected in feed-restricted alytesin-treated chicks. The anorexigenic effect of both ICV and peripheral alytesin may be mediated at the hypothalamus, since all hypothalamic nuclei studied; regio lateralis hypothalami, nucleus dorsomedialis hypothalami, nucleus paraventricularis magnocellularis, nucleus perventricularis hypothalami, nucleus infundibuli hypothalami and the nucleus ventromedialis hypothalami, were activated as evident by increased c-Fos immunoreactivity. Central alytesin did not cause increased behaviors that were unrelated to ingestion and did not cause anxiety-related behavior patterns. Additionally, central alytesin did not affect pecking efficacy. We conclude that both ICV and peripheral alytesin injections induce anorexigenic effects in chicks, and the hypothalamus is involved. While the anorexigenic effects of alytesin and bombesin appear to be conserved across species, the two peptides may differ in other behavioral responses and central mechanisms of action.

Anorexigenic effects of central neuropeptide K are associated with hypothalamic changes in juvenile Gallus gallus.

The central mechanisms that mediate neuropeptide K (NPK) associated anorexia are poorly understood in any species, and information in this area of avian biology is totally lacking. Thus, the effects of intracerebroventricular NPK treatment were studied in Cobb-500 chicks (Gallus gallus). In Experiment 1, NPK caused decreased feed intake, but did not affect water intake or whole blood glucose concentration. In Experiment 2, NPK-treated chicks had increased c-Fos immunoreactivity in the parvicellular division of the paraventricular nucleus and arcuate nucleus. The lateral hypothalamus, ventromedial hypothalamus, dorsomedial hypothalamus, periventricular nucleus, magnocellular division of the paraventricular nucleus, and the superchiasmatic nucleus were not affected by NPK treatment. In Experiment 3, the number of feed pecks, exploratory pecks, jumps, escape attempts, and distance moved were decreased, while time spent standing was increased. None of the NPK-treated chicks sat or entered deep rest. In Experiment 4, blockage of corticotrophin releasing factor receptors did not affect NPK-induced anorexia. Thus, we conclude that NPK is a regulator of chick appetite and the effects may be mediated directly in the arcuate nucleus and parvicellular division of the paraventricular nucleus.