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Artículo de publicación ISIA form of polycystic ovary (PCO) resembling some aspects of thehuman PCO syndrome can be induced in rats by a single injection ofestradiol valerate (EV). An increase in sympathetic outflow to theovary precedes, by several weeks, the appearance of cysts, suggestingthe involvement of a neurogenic component in the pathology of thisovarian dysfunction. The present study was carried out to test thehypotheses that this change in sympathetic tone is related to anaugmented production of ovarian nerve growth factor (NGF), and thatthis abnormally elevated production of NGF contributes to the formationof ovarian cysts induced by EV. Injection of the steroid resultedin increased intraovarian synthesis of NGF and its low affinityreceptor, p75 NGFR. The increase was maximal 30 days after EV,coinciding with the elevation in sympathetic tone to the ovary andpreceding the appearance of follicular cysts. Intraovarian injectionsof the retrograde tracer fluorogold combined with in situ hybridizationto detect tyrosine hydroxylase (TH) messenger RNA-containing neuronsin the celiac ganglion revealed that these changes in NGF/p75NGFR synthesis are accompanied by selective activation of noradrenergicneurons projecting to the ovary. The levels of RBT2 messengerRNA, which encodes a b-tubulin presumably involved in slowaxonal transport, were markedly elevated, indicating that EVinducedformation of ovarian cysts is preceded by functional activationof celiac ganglion neurons, including those innervating the ovary.Intraovarian administration of a neutralizing antiserum to NGF inconjunction with an antisense oligodeoxynucleotide to p75 NGFR, viaAlzet osmotic minipumps, restored estrous cyclicity and ovulatorycapacity in a majority of EV-treated rats. These functional changeswere accompanied by restoration of the number of antral follicles perovary that had been depleted by EV and a significant reduction in thenumber of both precystic follicles and follicular cysts. The resultsindicate that the hyperactivation of ovarian sympathetic nerves seenin EV-induced PCO is related to an overproduction of NGF and its lowaffinity receptor in the gland. They also suggest that activation of thisneurotrophic-neurogenic regulatory loop is a component of the pathologicalprocess by which EV induces cyst formation and anovulationin rodents. The possibility exists that a similar alteration in neurotrophicinput to the ovary contributes to the etiology and/or maintenanceof the PCO syndrome in humans. (Endocrinology 141: 1059–1072, 2000)Fondo Nacional de Ciencias deChile (Project 1961018) and The Rockefeller Foundation (to H.E.L.) andby NIH Grants HD-24870 (to S.R.O.), and P30 Population Center GrantHD-18185 and RR-00163 for the operation of the Oregon Regional PrimateResearch Center

endocrinology

An Increased Intraovarian Synthesis of Nerve Growth Factor and Its Low Affinity Receptor Is a Principal Component of Steroid-Induced Polycystic Ovary in the Rat