Ganglionic and ovarian action of acetylcholine during diestrous II in rats. Neuroendocrine control of the luteal regression.

Our aim was to investigate if acetylcholine (Ach), added to the celiac ganglion-superior ovarian nerve-ovary system (CG-SON-ovary) or in ovary incubations, modifies the release of progesterone (P4), androstenedione (A2), dopamine (DA), norepinephrine (NE), gonadotropin-releasing hormone (GnRH), and alters the expression of 3ß-hydroxysteroid dehydrogenase (3ß-HSD), 20α-hydroxysteroid dehydrogenase (20α-HSD), and apoptotic genes in ovarian tissue during the diestrous II (DII) in rats. The CG-SON-ovary system or the ovary alone were removed and placed into separate cuvettes both containing Krebs-Ringer solution (control groups). In experimental groups, 10-6 M Ach was added into the ganglion compartment or into the ovary compartment. P4, A2 and GnRH were measured by RIA, mRNA expression by RT-PCR, and catecholamines by HPLC. In addition, a routine histological technique was applied. In ex-vivo system, 10-6 M Ach into the ganglion compartment decreased P4 and NE release, altered 3ß-HSD and 20α-HSD expression, and decreased bax/bcl-2 ratio, while increasing the release of A2 and DA, and bcl-2 expression. In ovary incubations, 10-6 M Ach decreased P4 and GnRH release, decreased 3ß-HSD and bcl-2 expression, increased A2 release, increased 20α-HSD and bax expression, and the bax/bcl-2 ratio, and induced disorganization of the corpus luteum structure. The peripheral nervous system protected the ovary from the apoptotic mechanisms while in the ovary incubation the effect was reversed. Our results indicate that Ach in DII regulates steroidogenesis and apoptosis in the ovary, by modulating the concentration of neurotransmitters. In vivo, an alteration in the extrinsic cholinergic innervation of the ovary could disrupt the endocrine control of the reproductive function.

Noradrenaline modulates the presence of gonadotropin-releasing hormone in ovary. The importance of its interrelation on the ovarian steroidogenesis and apoptosis on dioestrus II in rat.

The aim of this work was to investigate if noradrenaline (NA), added in the coeliac ganglion -superior ovarian nerve- ovary system (CG-SON-O) and in ovary incubation, modifies the release of ovarian progesterone (P4), gonadotropin-releasing hormone (GnRH) and oestradiol (E2), and the expression of 3ß-HSD and 20α-HSD and proapoptotic bax and antiapoptotic bcl-2 on dioestrus II in the rat. The CG-SON-O system and the ovary were removed and placed in one cuvette containing Krebs-Ringer solution (control groups), and NA was added to the ganglion compartment in the ex vivo system and in the ovary compartment in the ovary incubation (experimental groups). P4, GnRH and E2 were measured by RIA, and gene expression was measured by RT-PCR. In the ex-vivo system, the release of ovarian P4 and GnRH and the expression of 3ß-HSD and bax decreased; E2 and bcl-2 increased, and the bax/bcl-2 ratio decreased. However, in the ovary incubation, P4, GnRH, the expression of 3ß-HSD and bax increased; E2, the expression of 20α-HSD and bcl-2 decreased while the bax/bcl-2 ratio increased, thus favoring apoptosis. The peripheral nervous system protected the ovary from the apoptotic mechanisms while in the ovary incubation the effect was reverted. Our results indicate that NA regulates ovarian steroidogenesis and apoptosis by modulating GnRH release from the coeliac ganglion and ovary, being NA a possible generator of a GnRH-gonadotropins axis in the ovary. This work is expected to contribute with new evidence of the clinical importance of catecholamines and GnRH in therapy and prevention of ovarian pathologies.