HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pati, D. Articles by Habibi, H. R. Search for Related Content PubMed PubMed Citation Articles by Pati, D. Articles by Habibi, H. R. Agricola Articles by Pati, D. Articles by Habibi, H. R.

Involvement of Protein Kinase C and Arachidonic Acid Pathways in the Gonadotropin-Releasing Hormone Regulation of Oocyte Meiosis and Follicular Steroidogenesis in the Goldfish Ovary¹

^a Department of Biological Sciences and Endocrine Research Group, University of Calgary, Calgary, Alberta, Canada T2N 1N4

The involvement of protein kinase C (PKC) and arachidonic acid (AA) pathways were investigated in the GnRH regulation of oocyte meiosis and follicular testosterone production in the goldfish ovary. The results clearly demonstrate differences in the postreceptor mechanisms involving the stimulatory and inhibitory actions of GnRH peptides on basal and gonadotropin (GtH)-induced reinitiation of oocyte meiosis and steroidogenesis. In isolated goldfish follicles in vitro, the observed stimulatory effects of both salmon GnRH (sGnRH) and chicken GnRH-II (cGnRH-II) on germinal vesicle breakdown were completely blocked by addition of PKC inhibitors, suggesting the involvement of PKC, presumably through activation of phospholipase C/diacylglycerol pathways in the GnRH-induced reinitiation of oocyte meiosis. Administration of an AA metabolism inhibitor, however, only blocked the stimulatory effect of sGnRH without affecting cGnRH-II-induced meiosis. As observed previously, in the presence of GtH, sGnRH was found to inhibit GtH-induced resumption of meiosis and testosterone production, whereas cGnRH-II was without effect. The inhibitory effect of sGnRH on GtH-induced meiosis and steroidogenesis was completely reversed by addition an AA metabolism inhibitor, whereas PKC inhibitors had no effect. These findings provide functional evidence in support of the novel hypothesis that goldfish ovarian follicles contain GnRH-receptor subtypes with different ligand selectivity mediating stimulatory and inhibitory actions of sGnRH and cGnRH in the goldfish ovary.

First decision: 18 September 2001.

¹ Supported by a Natural Sciences and Engineering Research Council Research Grant to H.R.H.

² Correspondence: H.R. Habibi, Department of Biological Sciences, University of Calgary, Calgary, AB, Canada T2N 1N4. FAX: 403 289 9311; habibi{at}ucalgary.ca

³ Current address: Texas Children's Cancer Center, Baylor College of Medicine, 6621 Fannin Street MC 3-3320, Houston, TX 77030-2399

This article has been cited by other articles:

				M. Liao, Y. Zhang, and M. L. Dufau Protein Kinase C{alpha}-Induced Derepression of the Human Luteinizing Hormone Receptor Gene Transcription through ERK-Mediated Release of HDAC1/Sin3A Repressor Complex from Sp1 Sites Mol. Endocrinol., June 1, 2008; 22(6): 1449 - 1463. [Abstract] [Full Text] [PDF]

				C. V. Andreu-Vieyra, A. G. Buret, and H. R. Habibi Gonadotropin-Releasing Hormone Induction of Apoptosis in the Testes of Goldfish (Carassius auratus) Endocrinology, March 1, 2005; 146(3): 1588 - 1596. [Abstract] [Full Text] [PDF]