Haruka Nishimura’s research while affiliated with Kyushu University and other places

Brain monoamines are reported to regulate body temperature and food intake. The objective of this study was to investigate the mechanism of brain monoamine metabolism in taurine-induced hypothermia and appetite suppression. In Experiment 1, 5-day-old male Julia layer chicks (n = 10) were subjected to intracerebroventricular (ICV) injection with saline or taurine (5 μmol/10 μL). In Experiment 2, the chicks were ICV injected with saline, taurine, fusaric acid (dopamine-β-hydroxylase inhibitor: 558 nmol), or taurine with fusaric acid. In Experiment 3, the chicks were ICV injected with saline, taurine, para-chlorophenylalanine (PCPA, tryptophan hydroxylase inhibitor: 400 nmol), or taurine with PCPA. In Experiment 4, the chicks were ICV injected with saline, taurine, clorgyline (monoamine oxidase inhibitor: 81 nmol), or taurine with clorgyline. Central taurine lowered rectal temperature at 30 min post-injection and increased norepinephrine in the brainstem and its metabolite 3-methoxy-4-hydroxyphenylglycol in both the diencephalon and brainstem. Similarly, taurine treatment induced increases in serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid in the diencephalon. Fusaric acid completely and PCPA partially, but not clorgyline, attenuated taurine-induced hypothermia. The anorexigenic effect of taurine was partially attenuated by PCPA, but not fusaric acid nor clorgyline. In conclusion, central taurine activates dopamine-β-hydroxylase and tryptophan hydroxylase to produce norepinephrine and 5-HT, and then induces hypothermia, but 5-HT alone may be linked with taurine-induced anorexia in chicks.

Previously it was found that mRNA expression of neuropeptide Y (NPY) was increased in the chicken brain under heat stress. NPY has also been reported as an anti-stress factor to regulate brain functions in heat exposed chicks. However, to the best of our knowledge, there is no report on the action of central NPY in the immune organs under heat stress. The aim of this study was to examine whether central injection of NPY can regulate heat stress response in the spleen and liver. After intracerebroventricular (ICV) injection of NPY, chicks were exposed to control thermoneutral temperature (CT: 30 ± 1°C) or high ambient temperature (HT: 35 ± 1°C) chambers for 60 min. Central injection of NPY caused lowering in rectal temperature under CT, but not under HT. Moreover, ICV injection of NPY caused a significant lower mRNA expression of heat-shock protein-70 and higher expression of glutathione synthase in the spleen, but not liver. Furthermore, plasma uric acid concentrations were significantly increased by the ICV injection of NPY in chicks under HT. These results indicate that brain NPY may contribute to attenuate the intracellular heat stress response and enhance antioxidative status in the immune organ, spleen in chicks.

High ambient temperatures (HT) in summer are becoming more severe due to global warming, leading to severe adverse effects on poultry production. Recently, we have reported that oral administration of L-citrulline (L-Cit) can minimize hyperthermia in chickens under HT. However, whether oral L-Cit can enter the brain, the center for thermoregulation, has not been studied. We investigated the effects of oral administration of L-Cit on free amino acids and monoamines in the diencephalon region of the brain of heat-exposed broilers. Broilers were treated with L-Cit (40 mmol/20 ml/bird), then moved to a chamber at HT (30 ± 1°C) or to a thermoneutral temperature (CT: 22 ± 1°C) chamber for 2 h. Control groups were given methyl cellulose solution and placed in the CT or HT chambers. After 2 h of exposure to HT, there were increased brain concentrations of Cit in comparison with concentrations in broilers exposed to CT, whereas brain ornithine (Orn) concentrations were decreased, and arginine (Arg) concentrations were not changed. Interestingly, oral administration of L-Cit increased brain concentration of Cit, Arg, and Orn under both CT and HT. Tryptophan and its metabolite, serotonin (5-HT) concentrations were lower in the brain under HT than under CT. HT did not change brain concentrations of tyrosine, but dopamine (DA, a metabolite of tyrosine) concentrations decreased, and methoxyhydroxyphenylglycol (MHPG, a metabolite of DA) concentrations increased in comparison with CT. Oral administration of L-Cit decreased brain concentrations of both tryptophan and tyrosine under CT and HT without changing 5-HT; however, DA levels declined under HT. Moreover, MHPG concentrations increased. In conclusion, these results suggest that metabolism of amino acids and metabolism of DA can be enhanced in the brain by oral administration of L-Cit. Metabolic changes in the brain in response to oral administration of L-Cit may influence the thermoregulatory center in the brain, leading to a reduction in body temperature and conferring thermotolerance in heat-exposed broiler chickens.