(PCO) in rats are associated with higher ovarian release and content of norepinephrine, decreased 2-adrenoceptors (ARs), and dysregulated expression of ␣1-AR subtypes, all preceded by an increase in the production of ovarian NGF. The aim of this study was to further elucidate the role of NGF in the ovaries by blocking the action of NGF during development of EV-induced PCO in rats. Control and EV-injected rats were treated with intraperitoneal injections of IgG (control and PCO groups) or with anti-NGF antibodies (anti-NGF and PCO anti-NGF groups) every third day for 5 wk starting from the day of PCO induction. Rat weight, estrous cyclicity, ovarian morphology, ovarian mRNA, and protein expression of ␣1-AR subtypes, 2-AR, the NGF receptor tyrosine kinase A (TrkA), p75 neurotrophin receptor (p75 NTR ), and tyrosine hydroxylase (TH) were analyzed. Ovaries in both PCO and PCO anti-NGF groups decreased in size as well as in number and size of corpora lutea. mRNA expression of ␣ 1a-AR and TrkA in the ovaries was lower, whereas expression of ␣ 1b-and ␣1d-AR and TH was higher, in the PCO group than in controls. Protein quantities of ␣ 1-ARs, TrkA, p75 NTR , and TH were higher in the PCO group compared with controls, whereas the protein content of  2-AR was lower. Anti-NGF treatment in the PCO group restored all changes in mRNA and protein content, except that of ␣ 1b-AR and TrkA mRNAs, to control levels. The results indicate that the NGF/NGF receptor system plays a role in the pathogenesis of EV-induced PCO in rats.nerve growth factors; sympathetic nervous system; ovarian innervation; tyrosine kinase A; p75 neutrophin receptor POLYCYSTIC OVARY SYNDROME (PCOS) is a heterogeneous condition of uncertain etiology that affects between 5% and 10% of women of reproductive age (41). PCOS is characterized by a myriad of symptoms and signs, which include ovulatory dysfunction, the presence of polycystic ovaries (PCO), abdominal obesity, hyperandrogenism, and in many cases hypertension and insulin resistance (41). Several theories have been proposed to explain the pathogenesis of PCOS, such as an enhanced production of ovarian androgens, an alteration in the metabolism of cortisol resulting in enhanced production of adrenal androgens, a defect in the action and secretion of insulin, and a neuroendocrine defect that causes an exaggeration in the pulse and frequency amplitude of LH (41).The involvement of the sympathetic nervous system in the etiology and maintenance of PCOS is suggested by both clinical and experimental findings (5,20,22,24,25). Ovarian function is known to be regulated by both hormonal and intraovarian signaling. It is also known that the sympathetic innervation of the ovary is involved in follicular development (23) and in ovarian steroidogenesis (1). That the sympathetic nervous system is involved in the pathophysiology of human PCOS is supported by the fact that the innervation of the catecholaminergic nerve fibers in the PCO of women with PCOS is more dense than in normal ovaries (18,35).Chronic anovulati...