NEW FUNCTIONS OF CLASSICAL HORMONE, α-MELANOPHORE- STIMULATING HORMONE

3) Abstract　It is well‑known that α‑melanophore‑stimulating hormone (α‑MSH) release from the amphibian pars intermedia (PI) depends on the light condition of the animals background. In the present study we present two new functions of α‑MSH in amphibians and mammals. In Xenopus laevis we show that temperatures below 8 ℃ stimulate α‑MSH secretion of the PI and skin darkening with a maximum at 5 ℃ under regulation of the hypothalamus rule independently from the illumination state of the background. The cold‑induced α‑MSH release of the PI was inhibited by neuropeptide‑Y‑producing suprachiasmatic‑melanotrope‑inhibiting neurons in the ventrolateral area of the suprachiasmatic nucleus but increasely in thyrotropin‑releasing‑hormene‑containing neurons of the magnocellular nucleus. It is known that intracerebroventricular (ICV) administration of a low dose of interleukin‑1β (IL‑1β) induces hyperalgesia in rat and that this eff ect can be inhibited by α‑MSH. To identify the part of the brain that is aff ected by hyperalgesia‑ inducing IL‑1β and the site of α‑MSH concerned we have examined Fos expression in the brain in response to ICV microinjection of α‑MSH and/or IL‑1β. Following injection of 10 pg IL‑1β hyperalgesia was induced and Fos became expressed in the paraventricular nucleus (PVN) of the hypothalamus and in the arcuate nucleus (ARC) which contains α‑MSH‑producing neurons. ICV co‑injection of IL‑1β ・ with 30 ng α‑MSH fully inhibited both hyperalgesia and Fos expression in the PVN and the ARC. We conclude that PVN neurons are activated by hyperalgesic IL‑1β and propose that this eff ect is abolished by α‑MSH released from the ARC but not from the pituitary gland. Hirosaki Med.J.　59 Supplement:S202―S209,2007