Ghrelin is a gut-brain peptide that has a stimulatory effect on food intake in mammals. In contrast, this peptide decreases food intake in neonatal chicks when injected intracerebroventricularly (ICV). In mammals, neuropeptide Y (NPY) mediates the orexigenic effect of ghrelin whereas in chicks it appears that corticotrophin releasing factor (CRF) is partially involved in the inhibitory effect of ghrelin on food intake. Gamma aminobutyric acid (GABA) has a stimulatory effect on food intake in mammals and birds. In this study we investigated whether the anorectic effect of ghrelin is mediated by the GABAergic system. In Experiment 1, 3h-fasted chicks were given an ICV injection of chicken ghrelin and picrotoxin, a GABA(A) receptors antagonist. Picrotoxin decreased food intake compared to the control chicks indicating a stimulatory effect of GABA(A) receptors on food intake. However, picrotoxin did not alter the inhibitory effect of ghrelin on food intake. In Experiment 2, THIP hydrochloride, a GABA(A) receptor agonist, was used in place of picrotoxin. THIP hydrochloride appeared to partially attenuate the decrease in food intake induced by ghrelin at 30 min postinjection. In Experiment 3, the effect of ICV injection of chicken ghrelin on gene expression of glutamate decarboxylase (GAD)(1) and GAD(2), GABA synthesis enzymes in the brain stem including hypothalamus, was investigated. The ICV injection of chicken ghrelin significantly reduced GAD(2) gene expression. These findings suggest that ghrelin may decrease food intake in neonatal chicks by reducing GABA synthesis and thereby GABA release within brain feeding centers.
"Inhibition of hypothalamic AMPK signalling was observed after central ghrelin injection in chickens (Xu et al., 2011) which is in contrast to the widely acknowledged stimulatory effect of ghrelin on AMPK signalling in the mammalian hypothalamus (Stark et al., 2013). Recently, ICV ghrelin injection was also shown to suppress gamma aminobutyric acid (GABA) synthesis in the neonate chick brain, further supporting an anorexigenic role for central ghrelin in birds (Jonaidi et al., 2012). These findings support the hypothesis that ghrelin plays an anorexigenic role in birds (Kaiya et al., 2013b). "
"The stimulant of ghrelin secretion in rainbow trout is not sure at present. In birds, ICV injected ghrelin always inhibits food intake in chickens and quail      . However, there are cases where different actions are seen when ghrelin injected IV in chickens: broiler shows inhibitory action   , and layers does not show any effect . "
[Show abstract][Hide abstract] ABSTRACT: Ten years and more passed since ghrelin was discovered. Various physiological actions of ghrelin have been documented in both mammalian and non-mammalian vertebrates. Do these actions have any commonality? In this review, we focused on several effects of ghrelin, and compared the effect across vertebrates. We would like to discuss possible general function of ghrelin in vertebrates.
General and Comparative Endocrinology 11/2012; 181(1). DOI:10.1016/j.ygcen.2012.10.015 · 2.47 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: 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.
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