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This Article Full Text Full Text (PDF) All Versions of this Article: 68/2/516    most recent biolreprod.102.009662v1 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 Google Scholar Google Scholar Articles by Patiño, R. Articles by Thomas, P. Search for Related Content PubMed PubMed Citation Articles by Patiño, R. Articles by Thomas, P. Agricola Articles by Patiño, R. Articles by Thomas, P.

Role of Arachidonic Acid and Protein Kinase C During Maturation-Inducing Hormone-Dependent Meiotic Resumption and Ovulation in Ovarian Follicles of Atlantic Croaker¹

^a U.S. Geological Survey, ^b Texas Cooperative Fish & Wildlife Research Unit, Texas Tech University, Lubbock, Texas 79409-2120 ^c Department of Aquatic Biosciences, Tokyo University of Fisheries, Minato-ku, Tokyo 108-8477, Japan ^d University of Texas Marine Science Institute, Port Aransas, Texas 78373-1267

The roles of arachidonic acid (AA) and protein kinase C (PKC) during in vitro maturation-inducing hormone (MIH)-dependent meiotic resumption (maturation) and ovulation were studied in ovarian follicles of Atlantic croaker (Micropogonias undulatus). The requirement for cyclooxygenase (COX) metabolites of AA was examined using a nonspecific COX inhibitor, indomethacin (IM), as well as two COX products, prostaglandin (PG) F₂ and PGE₂, whereas the role of lipoxygenase (LOX) was investigated using a specific LOX inhibitor, nordihydroguaiaretic acid (NDGA). The involvement of PKC was examined using phorbol 12-myristate 13-acetate (PMA), a PKC activator, as well as GF109203X (GF), a specific inhibitor of PKC and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7), nonspecific inhibitor of protein kinases. Genomic mechanisms were examined with the transcription-inhibitor actinomycin D (ActD) and the functionality of heterologous (oocyte-granulosa) gap junctions (GJ) with a dye transfer assay. The AA (100 µM) and PGF₂ (5 µM) did not induce maturation, and NDGA (10 µM) did not affect MIH-dependent maturation. However, IM (100 µM) partially inhibited MIH-dependent maturation. Conversely, AA and both PGs induced, and IM and NDGA inhibited, MIH-dependent ovulation in matured follicles. The PMA (1 µg/ml) did not induce maturation but caused ovulation in matured follicles, whereas PKC inhibitors (GF, 5 µM; H7, 50 µM) did not affect MIH-dependent maturation but inhibited MIH- and PMA-dependent ovulation. The PMA-dependent ovulation was inhibited by IM but not by NDGA. In addition, ActD (5 µM) blocked MIH-dependent, but not PMA-dependent, ovulation, and PGF₂ restored MIH-dependent ovulation in ActD-blocked follicles. The AA and PGs did not induce, and GF did not inhibit, MIH-dependent heterologous GJ uncoupling. In conclusion, AA and PKC mediate MIH-dependent ovulation but not meiotic resumption or heterologous GJ uncoupling in croaker follicles, but a permissive role of COX products of AA during maturation is possible. A novel model of MIH-dependent ovulation is proposed in which 1) LOX and COX metabolites of AA are both required for ovulation, but at upstream and downstream sites of the pathway, respectively, relative to PKC, and 2) PKC is downstream of genomic activation.

¹ Funding for this work was provided by the U.S. Department of Agriculture (NRICGP Animal Reproduction, 00-35203-9135) and Japan Society for the Promotion of Science's Research for the Future program (97L00902). The U.S. Geological Survey, Texas Tech University, Texas Parks and Wildlife Department, and the Wildlife Management Institute jointly sponsor the Texas Cooperative Fish and Wildlife Research Unit.

² Correspondence. FAX: 806 742 2946; r.patino{at}ttu.edu