Influence of peripheral lipopolysaccharide (LPS) on feed intake, body temperature and hypothalamic expression of neuropeptides involved in appetite regulation in broilers and layer chicks.

1. This study examined the expression of genes related to appetite-regulating neuropeptides in the hypothalamus of broiler and layer chicks (Gallus gallus) after intraperitoneal (IP) injection of lipopolysaccharide (LPS). 2. Both broiler and layer chicks received (n = 10 per group) LPS at doses of 0 and 200 µg and feed intake was measured up to 6 h after injection. In a further experiment, (n = 8 per group) mRNA abundance of some hypothalamic neuropeptides was measured 2 h after injection. The rectal temperature of each chick was measured before and 2 h post-injection. 3. Feed intake was significantly decreased by LPS from 2 h after injection and thereafter, while the rectal temperature did not change. 4. LPS decreased the expression of appetite-enhancing neuropeptides: neuropeptide Y (NPY) and agouti-related peptide (AgRP) in broilers and, NPY in layer chicks. The expression of appetite-suppressing neuropeptides (corticotrophin-releasing factor (CRF), proopiomelanocortin (POMC) and, cocaine and amphetamine regulated-transcript (CART) was not changed in broilers, while CRF tended to decrease and POMC was significantly decreased in layers. The abundance of the cytokine tumour necrosis factor-alpha (TNF-α) did not change in broilers but was decreased in layers. 5. The findings indicated that the reduction in gene expression of hypothalamic appetite-enhancing neuropeptides NPY and AgRP is responsible for anorexia caused by LPS at a dose that did not influence body temperature.

Induction of hypothalamic GABA synthetic enzymes mRNA (Gad 1 and Gad 2) expression by negative energy balance in broiler and layer chicks.

Broiler and layer chicks have been selected for higher and lower food intake and body weight gain, respectively. It has recently been reported that glutamate decarboxylase (Gad1) mRNA, a gamma-aminobutyric acid (GABA) synthetic enzyme gene, is a reliable proxy for GABA release. Previous studies have revealed that GABAergic system has a stimulatory role on food intake in both mammals and birds. Over the recent years, evidence has identified the presence of GABAergic neurons as either the first- or second-order neurons within the various feeding nuclei of hypothalamus of laboratory rodents. They respond to the negative energy balance representing a critical role for GABA in the regulation of food intake. In the current study, the mRNA abundance of Gad 1 and Gad 2 was measured within the hypothalamus of both broiler and layer free fed, 12 h-fasted and 12 h-fasted / 3 h refed chicks. Furthermore, the effect of intracerebroventricular (ICV) injection of GABA was studied on food intake of chicks. The results indicated an increase in both Gad 1 and 2 expressions during fasting which tended to return to the baseline after refeeding. However, this increase was greater in broilers than in layers. The results also showed that ICV injection of GABA had no effect on food intake with the exception of an increase in free fed broilers. This study suggests a role for hypothalamic GABAergic system in birds that respond to negative energy balance, which seems to be more considerable in broilers than in layers.

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.