Marissa L. Smith

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.

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.

Central α-melanocyte stimulating hormone attenuates behavioral effects of neuropeptide Y in chicks

This experiment was conducted to determine the effects of central alpha-melanocyte stimulating hormone (alpha-MSH) and its interaction with neuropeptide Y (NPY) on ingestive and non-ingestive behaviors in chicks. Chicks received intracerebroventricular injections of either 0, 0.12 nM alpha-MSH, 0.06 nM NPY, or 0.12 nM alpha-MSH+0.06 nM NPY. Immediately following injection, chicks were placed in an observation arena and the number of steps, jumps, feed pecks, drinks, exploratory pecks, escape attempts, the total distance traveled, and the amount of time spent standing, sitting, sleeping, and preening were monitored for 60 min. Chicks treated with NPY consumed 69% more feed than controls whereas alpha-MSH-treated chicks consumed 71% less. Feed intake of the NPY+alpha-MSH groups was similar to alpha-MSH-treated chicks at 66% less than aCSF-treated chicks. Differences in pecking were found and followed a similar pattern as feed intake. All treatments increased the amount of time chicks were in a sitting posture, and the alpha-MSH+NPY group spent more time sitting than alpha-MSH and NPY alone. The sitting response after alpha-MSH+NPY treatment was similar to the alpha-MSH group but not the NPY group. Other behaviors were not affected by treatment. Thus, we conclude that alpha-MSH, at a concentration that causes a similar magnitude decrease in feed intake as NPY increases feed intake, is a more potent appetite-related signal than NPY. alpha-MSH causes behavioral effects that may secondarily affect feed intake at a low magnitude and may modulate the behavioral effects of NPY in chicks, contributing to the overall effect on feed intake.

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.

Amylin causes anorexigenic effects via the hypothalamus and brain stem in chicks.

This study was conducted to determine the effects of amylin on appetite-related processes in chicks. Broiler chicks were centrally and peripherally injected with amylin, and feed and water intake were quantified. Feed intake was reduced after both central and peripheral amylin, but water intake was not affected. To determine if the hypothalamus and brainstem were involved in the anorexigenic effect, chicks were centrally and peripherally injected with amylin, and c-Fos immunoreactivity was quantified in the lateral hypothalamus (LH), ventromedial hypothalamus (VMH), area postrema (AP) and the nucleus of the solitary tract (NTS). Amylin decreased c-Fos immunoreactivity in the LH, did not affect the VMH, and increased c-Fos immunoreactivity in the AP and NTS. To determine if alimentary transit time was affected, chicks received central amylin and were gavaged with chicken feed slurry containing a visible marker. Amylin-treated chicks had increased alimentary canal transit time. Chicks also responded to central amylin with increased anxiety-related behaviors and increased plasma corticosterone concentration. These results demonstrate that amylin affects feeding, alimentary canal transit, and behavior through hypothalamic and brainstem mechanisms in chicks.

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.

The Anorectic Effect of Neuropeptide AF is Associated with Satiety-Related Hypothalamic Nuclei

Neuropeptide AF (NPAF), a member of the RFamide family, is encoded by the same gene as neuropeptide FF (NPFF), which causes short‐term anorexia. However, reports on the role of NPAF on appetite‐related process are lacking. Thus, i.c.v. injections of 4.0, 8.0 and 16.0 nmol NPAF were administered to chicks to observe its effect on food and water intake. Chicks treated with 8.0 and 16.0 nmol i.c.v. NPAF decreased both their food and water intake. Additionally, all doses of NPAF injected caused a similar reduction in whole blood glucose concentration 180 min after injection. In a second experiment, chicks that received i.c.v. NPAF had an increased number of c‐Fos immunoreactive cells in the dorsomedial, paraventricular (magnocellular and parvicellular parts) and ventromedial nuclei. The arcuate nucleus and lateral hypothalamic area were not affected. In a third experiment, NPAF‐treated chicks exhibited fewer feeding pecks and spent less time perching, whereas they spent an increased time in deep rest. Other behaviours, including exploratory pecking, escape attempts, defecations, distance moved, and time spent standing, sitting and preening, were not affected by NPAF injection. We conclude that NPAF causes anorectic effects that are associated with the hypothalamus.

Both calcitonin and calcitonin gene-related peptides' thresholds of hypophagia are considerably lower in chicks selected for high rather than low juvenile body weight.

Effects of intracerebroventricular (ICV) injection of calcitonin (CT) and calcitonin gene-related peptide (CGRP) on food and water intake were measured in two lines of White Plymouth Rock chickens from a common base population that have undergone long-term divergent selection for either low (LWS) or high (HWS) juvenile body weight. These lines contain anorexic and obese individuals and serve as models for hypo- and hyperphagia. For both ICV injection of CT and CGRP, line HWS responded to a lower dose with decreased food intake than did line LWS. Both peptides were also associated with reduced water intake in both lines. Although plasma glucose concentrations were inherently different between lines, neither CT nor CGRP affected these levels. Comprehensive behavior analyses were conducted and only the number of food pecks was differentially suppressed between lines after both CT and CGRP injection. Thus, the selection program may have caused alterations in the endogenous CT and CGRP systems that synergistically, with other neurotransmitter systems, contribute to the role of food intake on the differential body weights between these lines.

Gamma(2)-melanocyte stimulating hormone decreases food intake in chicks.

The role of gamma melanocyte stimulating hormone (gamma-MSH) in appetite regulation is controversial in mammals and to our knowledge unreported within the avian class. Thus, the present study was designed to determine the effects of intracerebroventricularly (i.c.v.) administered gamma2-MSH on food intake using Cobb-500 chicks as models. In Experiment 1, chicks that received i.c.v. gamma2-MSH decreased their food intake throughout the 180 min observation period and plasma glucose concentration was not affected. Water intake was also decreased in i.c.v. gamma2-MSH-treated chicks, but only from 30 to 90 min post-injection. In Experiment 2, food pecking efficiency was decreased in i.c.v. gamma2-MSH-treated chicks and the amount of time spent sitting was increased. Other behaviors were not significantly affected by i.c.v. gamma2-MSH including distance traveled, the number of jumps, escape attempts, defecations, food pecks, exploratory pecks, and the amount of time spent standing, preening, perching, or in deep rest. These data suggest that gamma2-MSH is associated with anorexigenic effects and because of gamma-MSHs selectivity, implicates the melanocortin 3 receptor in appetite regulation.