LAUSR

In contrast to mammals, birds have higher basal metabolic rate and undertake wide range of energy-demanding activities. As a consequence, food deprivation to birds, even for a short-period, poses major energy challenge. The energy-regulating hypothalamic homeostatic mechanisms, although extensively studied in mammals, are far from clear in the case of birds. We focus on the interplay between neuropeptide Y (NPY) and thyrotropin-releasing hormone (TRH), two of the most important hypothalamic signaling agents, in modulating the energy balance in a bird model, zebra finch, Taeniopygia guttata. TRH neurons were confined to a few nuclei in the preoptic area and hypothalamus, and fibers widely distributed. Majority of TRH neurons in the hypothalamic paraventricular nucleus (PVN) whose axons terminate in median eminence were contacted by NPY-containing axons. Compared to fed animals, fasting significantly reduced body-weight, PVN pro-TRH-mRNA and TRH-immunoreactivity, but increased NPY-mRNA and NPY-immunoreactivity in the infundibular nucleus [IN, avian homolog of mammalian arcuate nucleus] and PVN. Refeeding for short duration restored PVN pro-TRH- and IN NPY-mRNA, and PVN NPY innervation to fed levels. Compared to control tissues, treatment of the hypothalamic superfused slices with NPY or an NPY-Y1 receptor agonist significantly reduced TRH-immunoreactivity, a response blocked by treatment with Y1-receptor antagonist. We describe a detailed neuroanatomical map of TRH-equipped elements, identify new TRH-producing neuronal groups in the avian brain, and demonstrate rapid restoration of the fasting-induced suppression of PVN TRH following refeeding. We further show that NPY via Y1 receptors may regulate PVN TRH neurons to control energy balance in T. guttata.