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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-09-0330v1 203/3/389    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Tanaka, M. Articles by Matsuda, K. PubMed PubMed Citation Articles by Tanaka, M. Articles by Matsuda, K.

Laboratory of Regulatory Biology, Graduate School of Science and Engineering, University of Toyama, 3190-Gofuku, Toyama 930-8555, Japan
¹ Graduate School of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima, Hiroshima 739-8521, Japan
² School of Marine Biosciences, Kitasato University, Ofunato, Iwate 022-0101, Japan
³ Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo 142-8555, Japan

(Correspondence should be addressed to K Matsuda; Email: kmatsuda{at}sci.u-toyama.ac.jp)

^* (M Tanaka and M Azuma contributed equally to this work)

Melanin-concentrating hormone (MCH)-containing neurons directly innervate the adenohypophysis in the teleost pituitary. We examined immunohistochemically the relationship between MCH-containing nerve fibres or endings and somatolactin (SL)-producing cells in the goldfish pituitary. Nerve fibres or endings with MCH-like immunoreactivity were identified in the neurohypophysis in close proximity to the adenohypophysial cells showing SL-like immunoreactivity. We also examined the effect of MCH on SL release from cultured goldfish pituitary cells and SL synthesis using a cell immunoblot and a real-time PCR method. Treatment of individually dispersed pituitary cells with MCH 10^–7 M for 3 h decreased the area of SL-like immunoreactivity on immunoblots, and MCH-induced reductions in SL release were blocked by treatment with the mammalian MCH receptor (MCHR) antagonist, compound-30, at a concentration of 10^–5 M. Treatment with 10^–7 M MCH for 3 h did not affect sl- and -β (smtla and -b as given in the Zfin Database) mRNA expression levels. These led us to explore the signal transduction mechanism leading to the inhibition of SL release, for which we examined whether MCH-induced reductions in SL release are mediated by the G_i or G_q protein-coupled signalling pathway. The MCH-induced reductions in SL release were abolished by treatment with the G_i/o protein inhibitors, NF023 (10^–5 M) or pertussis toxin (260 ng/ml), but not by the phospholipase C inhibitor, U-73122 (3x10^–6 M). These results indicate that MCH can potentially function as a hypothalamic factor suppressing SL release via the MCHR, and subsequently through the G_i protein to inhibit the adenylate cyclase/cAMP/protein kinase A-signalling pathway in goldfish pituitary cells.