ESTRADIOL PROMOTES LUTEAL REGRESSION IN THE LATE PREGNANT RAT THROUGH A DIRECT EFFECT IN THE OVARY AND AN INDIRECT EFFECT FROM THE CELIAC GANGLION VIA THE SUPERIOR OVARIAN NERVE

MARILINA CASAIS, ; SANDRA SILVINA VALLCANERAS,; FIORELLA CAMPO VERDE ARBOCCO,; SILVIA MARCELA DELGADO, ; MARIA BELÉN HAPON, ; ZULEMA SOSA, ; CARLOS TELLERIA,; ANA MARÍA RASTRILLA.

REPRODUCTIVE SCIENCES

SAGE PUBLICATIONS INC

Lugar: Thousand Oaks, California.; Año: 2012 p. 416 - 422

1933-7191

There is evidence suggesting that estradiol (E2) regulates the physiology of the ovary and the sympathetic neurons associated with the reproductive function. The objective of this study was to investigate the effect of E2 on the function of late pregnant rat ovaries, acting either directly on the ovarian tissue or indirectly via the superior ovarian nerve (SON) fromthe celiac ganglion (CG).Weused in vitro ovary (OV) or ex vivo CG-SON-OV incubation systems from day 21 pregnant rats. Various concentrations of E2 were added to the incubation media of either theOValone or the ganglion compartment of theCG-SON-OV system. In both experimental schemes, we measured the concentration of progesterone in the OV incubation media by radioimmunoassay at different times. Luteal messenger RNA (mRNA) expression of 3b-hydroxysteroid dehydrogenase (3b-HSD) and 20a-hydroxysteroid dehydrogenase (20a-HSD) enzymes, respectively, involved in progesterone synthesis and catabolism, and of antiapoptotic B-cell lymphoma 2 (Bcl-2) and proapoptotic Bcl-2-associated X protein (Bax), were measured by reverse transcriptase?polymerase chain reaction (RT-PCR) at the end of the incubation period. Estradiol added directly to theOVincubationor totheCGof theCG-SON-OVsystemcaused a decline in the concentration of progesterone accumulated in the incubation media. In addition, E2, when added to the OVincubation, decreased the expression of 3b-HSDand the ratio of Bcl-2/Bax.We conclude that through a direct effect on theOV, E2 favors luteal regression at the end of pregnancy in rats, in association with neural modulation from the CG via the SON.