PARENT SESSION
COMPARATIVE REPRODUCTION

Monday, August 2, 2004
10:30 AM–12:30 PM
Buchanan Courtyard

(110) ROLE OF ARACHIDONIC ACID IN THE EXPRESSION OF GROWTH HORMONE (GH) AND GONADOTROPIN SUBUNITS EXPRESSION IN THE GOLDFISH PITUITARY.

Pang , Flora ¹, Chang, John², Habibi, Hamid ¹, ¹ Departmant of Biological Sciences, University of Calgary, Calgary, AB, Canada² Departmant of Biological Sciences, University of Alberta, Edmonton, AB, Canada

ABSTRACT- Gonadotropin-releasing hormone (GnRH) is a key regulator of reproduction in vertebrates. Multiple forms of GnRH have been characterized and there is evidence for the presence of more than one GnRH variant in the brain of single species. Goldfish contains two molecular forms of GnRH, salmon (s)GnRH and chicken (c)GnRH-II. Both GnRH forms stimulate gonadotropin (GTH) and growth hormone (GH) release and gene expression in the goldfish pituitary. While considerable information is available on the mechanisms of GnRH-induced GTH and GH release, relatively limited information is available on the mechanisms of GnRH stimulated GTH subunits and GH synthesis. There is clear evidence that both sGnRH and cGnRH-II stimulate GTH and GH release via activation of Ca2+ dependent phospholipase C and protein kinase C. In addition, sGnRH-induced GTH release was found to involve arachidonic acid (AA) mobilization; sGnRH-induced GH release is not mediated by AA. In the present study, we investigated the involvement of AA on the regulation of sGnRH-mediated control of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and GH gene expression in the cultured goldfish pituitary cells. Treatment with sGnRH was found to stimulate LH- and GH mRNA levels in the goldfish pituitary. Small increase in FSH- mRNA level was also observed following treatment with sGnRH, although the differences were not statistically significant. In the same experiment, treatment with increasing concentrations of AA was without effect on LH-, FSH- and GH mRNA levels in the goldfish pituitary. Nor was treatment with an AA pathway inhibitor (5,8,11,13-ei-cosatetrayonic acid, ETYA) affected GnRH induced GTH subunit or GH mRNA levels in the goldfish pituitary. The findings provide a support for the hypothesis that the mechanism of sGnRH-mediated GTH subunit and GH gene expression does not involve mobilization of AA in the sexually regressed goldfish pituitary. Based on the present results, however, we cannot rule of the involvement of AA in the mechanism of GnRH action in sexually mature goldfish. Support by NSERC.

KEY WORDS: Arachidonic acid, Growth hormone , GnRH , Gonadotropin