Abstract

The functioning of the ovary is influenced by the autonomic system (sympathetic and cholinergic intraovarian system) which contributes to the regulation of steroid secretion, follicular development, and ovulation. There is no information on the primary signal that activates both systems. The nerve growth factor (NGF) was the first neurotrophic factor found to regulate ovarian noradrenergic neurons and the cholinergic neurons in the central nervous system. The aim of this study was to determine whether NGF is one of the participating neurotrophic factors in the activation of the sympathetic and cholinergic system of the ovary in vivo and its role in follicular development during normal or pathological states. The administration of estradiol valerate (a polycystic ovary [PCO] phenotype model) increased norepinephrine (NE) (through an NGF-dependent mechanism) and acetylcholine (ACh) levels. Intraovarian exposure of rats for 28 days to NGF (by means of an osmotic minipump) increased the expression of tyrosine hydroxylase and acetylcholinesterase (AChE, the enzyme that degrades ACh) without affecting enzyme activity but reduced ovarian ACh levels. In vitro exposure of the ovary to NGF (100 ng/ml for 3 h) increased both choline acetyl transferase and vesicular ACh transporter expression in the ovary, with no effect in ACh level. In vivo NGF led to an anovulatory condition with the appearance of follicular cysts and decreased number of corpora lutea (corresponding to noradrenergic activation). To determine whether the predominance of a NE-induced polycystic condition after NGF is responsible for the PCO phenotype, rats were exposed to an intraovarian administration of carbachol (100 μM), a muscarinic cholinergic agonist not degraded by AChE. Decreased the number of follicular cysts and increased the number of corpora lutea, reinforcing that cholinergic activity of the ovary participates in controlling its functions. Although NGF increased the biosynthetic capacity for ACh, it was not available to act in the ovary. Hence, NGF also regulates the ovarian cholinergic system, implying that NGF is the main regulator of the dual autonomic control. These findings highlight the need for research in the treatment of PCO syndrome by modification of locally produced ACh as an in vivo regulator of follicular development.

Highlights

  • Many studies have shown that ovary function is controlled by the sympathetic nervous system regulating steroid secretion, follicular development, and ovulation [1]

  • A previous report showed that after 30 days of estradiol valerate (EV) exposure, there was an increase in nerve growth factor (NGF) level in the ovary; 60 days after EV, there was an increase in norepinephrine level [17]

  • We found that ovarian ACh levels had increased ([mean ± SEM] 5.0 ± 0.6 μmol/mg ovary for sham vs. 12.3 ± 3.1 μmol/ovary for EV-treated rats, p < 0.05, unpaired MannWhitney test, n = 5)

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Summary

Introduction

Many studies have shown that ovary function is controlled by the sympathetic nervous system regulating steroid secretion, follicular development, and ovulation [1]. We have previously shown that the intraovarian cholinergic system mainly participates in the control of follicular development ovulation and atresia of antral follicles [6] Both noradrenergic and cholinergic systems regulate ovarian functions, probably working together or participating in a balanced way to regulate ovary function, similar to the autonomous regulation of many internal organs of the body [6]. NGF is one of the most important factors in the regulation of cholinergic neurons in the central nervous system [9, 10], but there is limited information on its action in the ovary If this is correct, we either can suggest that NGF acting on sympathetic nerves increases NE in the ovary by a direct effect of NGF or induced by stress [11, 12] and can participates in the development of the PCO phenotype in rat. It probably acts increasing the ACh concentration whose participation in ovary physiology is just recently been considered [4, 13]; much less is know in pathological conditions such as the PCO phenotype in rat

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