RESUMEN
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, 10-6â¯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, 10-6â¯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, 10-6â¯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.