HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Accepted manuscript (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.

M Tanaka, Laboratory of Regulatory Biology, University of Toyama, Toyama, Japan
M Azuma, Laboratory of Regulatory Biology, University of Toyama, Toyama, Japan
Y Nejigaki, Laboratory of Regulatory Biology, University of Toyama, Toyama, Japan
Y Saito, Graduate School of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima, Japan
K Mizusawa, School of Marine Biosciences, Kitasato University, Ofunato, Japan
M Uchiyama, Laboratory of Regulatory Biology, University of Toyama, Toyama, Japan
A Takahashi, School of Marine Biosciences, Kitasato University, Ofunato, Japan
S Shioda, Department of Anatomy, howa University School of Medicine, Shinagawa-ku, Japan
K Matsuda, Laboratory of Regulatory Biology, University of Toyama, Toyama, 930-8555, Japan

Correspondence: Kouhei Matsuda, Email: kmatsuda{at}sci.u-toyama.ac.jp

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 (MCH-R) 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 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 Gi or Gq protein-coupled signaling pathway. The MCH-induced reductions in SL release were abolished by treatment with the Gi/o protein inhibitors, NF023 (10-5 M) or pertussis toxin (260 ng/ml), but not by the phospholipase C inhibitor, U-73122 (3 x 10-6 M). These results indicate that MCH can potentially function as a hypothalamic factor suppressing SL release via the MCH-R, and subsequently through the Gi protein to inhibit the adenylate cyclase/cAMP/protein kinase A-signaling pathway in goldfish pituitary cells.