Research

Effect of electro-acupuncture on ovarian expression of α (1)- and β (2)-adrenoceptors, and p75 neurotrophin receptors in rats with steroid-induced polycystic ovaries

Luigi Manni^1,2 , Thomas Lundeberg³ , Agneta Holmäng¹ , Luigi Aloe² and Elisabet Stener-Victorin^1,4,5

¹  Cardiovascular Institute and Wallenberg Laboratory, Sahlgrenska Academy, Göteborg University, SE-413 45 Göteborg, Sweden

²  Institute of Neurobiology and Molecular Medicine (CNR), Rome, Italy

³  Rehabilitation Medicine, Karolinska Hospital, SE-171 77 Stockholm, Sweden

⁴  Department of Obstetrics and Gynaecology, Sahlgrenska University Hospital, Sahlgrenska, SE-413 45 Göteborg, Sweden

⁵  Institute of Occupational Therapy and Physical Therapy, Sahlgrenska Academy, Göteborg University, SE-405 30 Göteborg, Sweden

author email corresponding author email

Reproductive Biology and Endocrinology 2005, 3:21doi:10.1186/1477-7827-3-21

Published:	7 June 2005

Abstract

Background

Estradiol valerate (EV)-induced polycystic ovaries (PCO) in rats is associated with an increase in ovarian sympathetic outflow. Low-frequency (2 Hz) electro-acupuncture (EA) has been shown to modulate sympathetic markers as well as ovarian blood flow as a reflex response via the ovarian sympathetic nerves, in rats with EV-induced PCO.

Methods

In the present study, we further tested the hypothesis that repeated 2 Hz EA treatments modulate ovarian sympathetic outflow in rats with PCO, induced by a single i.m. injection of EV, by investigating the mRNA expression, the amount and distribution of proteins of α1a-, α1b-, α1d-, and β2-adrenoceptors (ARs), as well as the low-affinity neurotrophin receptor (p75NTR).

Results

It was found that EV injection results in significantly higher mRNA expression of ovarian α1b- and α1d-AR in PCO rats compared to control rats. The p75NTR and β2-ARs mRNA expression were unchanged in the PCO ovary. Low-frequency EA resulted in a significantly lower expression of β2-ARs mRNA expression in PCO rats. The p75NTR mRNA was unaffected in both PCO and control rats. PCO ovaries displayed significantly higher amount of protein of α1a-, α1b- and α1d-ARs, and of p75NTR, compared to control rats, that were all counteracted by repeated low-frequency EA treatments, except for α1b-AR.

Conclusion

The present study shows that EA normalizes most of the EV-induced changes in ovarian ARs. Furthermore, EA was able to prevent the EV-induced up regulation of p75NTR, probably by normalizing the sympathetic ovarian response to NGF action. Our data indicate a possible role of EA in the regulation of ovarian responsiveness to sympathetic inputs and depict a possible complementary therapeutic approach to overcoming sympathetic-related anovulation in women with PCOS.