Effects of pharmacological inhibition of signal transduction pathways in steroid-induced oocyte maturation in rainbow trout

Gonadotropins, steroids and insulin family growth factors act throughout the follicle-oocyte complex to regulate ovarian follicle maturation. Induction of oocyte maturation by the maturation inducing hormone (MIH) and insulin/insulin-like growth factor (IGF) peptides have received the most attention in lower vertebrates. The actions and receptor signaling pathways of these hormones often overlap and vary among species. The phosphatidylinositol-3 kinase (Pi3K) pathway, a primary signaling pathway for growth factors, is required not only for growth factor actions, but also for optimal gonadotropin and MIH induction of oocyte maturation in many fish species. The species-specific involvement of the Pi3K pathway in the integration of growth factor and MIH induction of ovarian follicle maturation and oocyte maturation is not well understood. Discovering the physiological basis for this variation will contribute to understanding the evolution of diverse reproductive strategies among fishes. Rainbow trout, ( Oncorhynchus mykiss ), appear unusual in that insulin and IGFs cannot induce resumption of meiosis or competence of the oocyte to respond to the MIH, 17,20βP, making it an interesting species to investigate Pi3K pathway signaling by MIH. In the present study, 17,20βP induction of meiosis resumption and Mapk activation were blocked or attenuated by pharmacological inhibition of Pi3K (wortmannin, LY294002) or Mek (PD98059, U0126), but were not affected by inhibitors of Akt (ML-9) or mTOR (rapamycin). The results indicate Pi3K and Mapk activation are required for optimal MIH-induction of meiosis resumption in rainbow trout follicles and may be required in other fishes in which insulin or IGFs do not directly induce competence or oocyte maturation. • MIH but not IGF1 induced GVBD and activation of Mapk1/3. • MIH-induced GVBD was attenuated by inhibitors of Mek and Pi3K but not Akt or mTOR. • Levels of activated Mapk1/3 were higher at GVBD than at 24 h after MIH stimulation. • MIH-induced activation of Mapk1/3 was attenuated by inhibitors of Pi3K.