Abstract

Estradiol (E2) accelerates oviductal egg transport through intraoviductal non-genomic pathways in unmated rats and through genomic pathways in mated rats. This shift in pathways has been designated as intracellular path shifting (IPS), and represents a novel and hitherto unrecognized effect of mating on the female reproductive tract. We had reported previously that IPS involves shutting down the E2 non-genomic pathway up- and downstream of 2-methoxyestradiol. Here, we evaluated whether IPS involves changes in the genomic pathway too. Using microarray analysis, we found that a common group of genes changed its expression in response to E2 in unmated and mated rats, indicating that an E2 genomic signaling pathway is present before and after mating; however, a group of genes decreased its expression only in mated rats and another group of genes increased its expression only in unmated rats. We evaluated the possibility that this difference is a consequence of an E2 non-genomic signaling pathway present in unmated rats, but not in mated rats. Mating shuts down this E2 non-genomic signaling pathway up- and downstream of cAMP production. The Star level is increased by E2 in unmated rats, but not in mated rats. This is blocked by the antagonist of estrogen receptor ICI 182 780, the adenylyl cyclase inhibitor SQ 22536, and the catechol-O-methyltransferase inhibitor, OR 486. These results indicate that the E2-induced gene expression profile in the rat oviduct differs before and after mating, and this difference is probably mediated by an E2 non-genomic signaling pathway operating on gene expression only in unmated rats. © 2010 Society for Reproduction and Fertility.