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Pigment-dispersing activities and cortisol-releasing activities of melanocortins and their receptors in xanthophores and head kidneys of the goldfish Carassius auratus

AuthorsKobayashi, Yuki; Chiba, Hiroaki; Mizusawa, Kanta; Suzuki, Nobuo; Cerdá-Reverter, José Miguel ; Takahashi, Akiyoshi
Issue Date2011
PublisherAcademic Press
CitationGeneral and Comparative Endocrinology 173(3): 438-446 (2011)
AbstractThe five subtypes of melanocortin receptors (MCRs) mediate the functions of α-melanocyte-stimulating hormone (α-MSH) and adrenocorticotropic hormone (ACTH). In fish, these hormones are involved in pigment dispersion and cortisol release, respectively. α-MSH-related peptides exhibit ACTH-like activity in certain fishes. We recently found that multiple Mcr transcripts are expressed in some cell types in the barfin flounder, which is related to regulation of α-MSH activities. Similar results were also observed for the cortisol-releasing activity of α-MSH-related peptides in the head kidney. The present study was undertaken to assess relationship between the expression of multiply expressed Mcrs and α-MSH activities using goldfish. We also determined if α-MSH-related peptides exhibit ACTH-like activity in goldfish. The transcripts of Mc1r, but not those of other subtypes, were observed in xanthophores. α-MSH, which has an acetyl group at the N-terminus, was found to disperse pigment in a dose-dependent manner in xanthophores. This potency was found to be slightly greater than that of desacetyl-α-MSH. These results support our findings that MCR has a higher affinity for α-MSH when single Mcr subtype is expressed. On the other hand, transcripts of Mc2r, but not those of other subtypes, were observed in the head kidney. ACTH1-24-stimulated cortisol release was observed in a dose-dependent manner, while α-MSH-related peptides showed no activity. It therefore appears that MC2R also acts as an ACTH-specific receptor in goldfish and that association of α-MSH-related peptides upon release of cortisol is uncommon in fishes. © 2011 Elsevier Inc.
Identifiersdoi: 10.1016/j.ygcen.2011.06.019
issn: 0016-6480
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