Voluminous literature about the neuroendocrine mechanism of

Voluminous literature about the neuroendocrine mechanism of reproduction and energy regulation has emerged from studies involving mammalian species. The avian infundibular nucleus (equivalent structure to the mammalian arcuate nucleus) consists of two neuronal populations, one of which expresses neuropeptide Y (NPY) and agouti-related protein (AgRP) [7] and the other pro-opiomelanocortin (POMC) and cocaine-and amphetamine-regulated transcript (CART). These two neuronal subsets potentially regulate the reproduction and energy homeostasis [8] by exerting potential anabolic (NPY and AGRP) and catabolic (POMC and CART) effects [9]. Hypothalamic expression of NPY in poultry psoralen sale responds to changes in energy status caused by fasting, feed restriction and energy expenditure [10]. Moreover, NPY has been shown to be a potent orexigenic agent in poultry birds when administered centrally [11,12]. On the other hand, β-endorphin, a POMC cleaved peptide, has been suggested to exert a tonic inhibitory effect upon hypothalamic GnRH secretion, which is well documented in many species of mature animals, including domestic hens [13]. Interestingly, melanocortin receptors MC3R and MC4R are present on the GnRH neurons [14] and can directly be modulated through the melanocortin and NPY signals/inputs [15], suggesting this as a possible route of regulation of the energy balance and reproductive axis. CART plays an important role in regulating the feeding in fishes [16], birds [[17], [18], [19]] and mammals [20]. The anorexic effect of CART may be different between fasting and NPY-induced feeding. It is also reported that layer chicks are more sensitive to AgRP than broiler chicks and CART is not capable of suppressing the AgRP induced feeding. CART, when, injected intra-cerebroventricularly, strongly inhibits feeding in broilers while weakly influences the food intake in layer chicks following fasting [18]. In our previous study, significantly increased hypothalamic GnRH is documented in PS and SR quail, while, PR and SS quail showed significantly increased hypothalamic GnIH and Mel1cR [21]. The increase in pulsatile GnRH release is mediated by interactions between neuropeptides and various peripheral hormones that integrate and act at the hypothalamic level [22]. NPY and POMC are two putative neuronal inputs, contributing their projections to GnRH neuronal terminals at the medial eminence and are involved in the regulation of reproduction [15] and food intake [23]. GnRH neurons, in adult mammals, express receptors for NPY [24], and receive appositions from CART [25]. It is also reported that the testicular stimulation induced by long-day conditions preceded hypothalamic IR mRNA induction which can be abolished by castration but can be rescued, administering within a physiological dose of testosterone under short-day conditions in quail [26]. Adiponectin stimulates food intake in mice via activation of AMPK [27,28]. Receptors for this orexigenic hormone were abundantly expressed in the paraventricular hypothalamus [29,30]. Adiponectin stimulates glucose utilization and fatty acid oxidation [30] through AMPK activation which mediates the ATP production and restores the AMP:ATP ratio [31]. The central and peripheral nutrient signals do not directly influence the NPY/AgRP or POMC neurons rather induce a presynaptic positive feedback loop involving AMPK and generate an excitatory or inhibitory synaptic input on these orectic/anorectic neurons [32]. Guillod-Maximin and co-workers demonstrated the colocalization of AdipoR1/AdipoR2 with both POMC and NPY neurons in rat arcuate nucleus [33]. Despite the marked progress made in mammalian studies, as yet, the alterations in hypothalamic food-intake regulatory neuropeptides, insulin receptor, adiponectin receptors and AMPK-pAMPK system in photo-influenced avian species is poorly understood, especially in relation to neuroendocrine mechanism(s) of energy regulation in quail exhibiting different photoperiodic phenotypes.