Neuroendocrinology
Original Paper
Synergistic Induction of Aromatase Activity in the Rat Brain by Estradiol and 5α-DihydrotestosteroneRoselli C.E.Department of Physiology, Oregon Health Sciences University, Portland, Oreg., and Division of Reproductive Biology and Behavior, Oregon Regional Primate Research Center, Beaverton, Oreg., USA
|
|
Log in to MyKarger to check if you already have access to this content.
KAB
Buy a Karger Article Bundle (KAB) and profit from a discount!
If you would like to redeem your KAB credit, please log in.
Save over 20% compared to the individual article price.
Article / Publication Details
Received: April 17, 1990
Accepted: June 22, 1990
Published online: April 04, 2008
Issue release date: 1991
Number of Print Pages: 6
Number of Figures: 0
Number of Tables: 0
ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)
For additional information: https://www.karger.com/NEN
Abstract
Estrogens are produced locally from androgen precursors by cells within the hypothalamus and preoptic area (POA). The activity of the aromatase enzyme complex responsible for this intracellular conversion is controlled by gonadal steroids. The purpose of this study was to determine: whether estrogen acts together with androgen to regulate aromatase activity (AA) and whether nuclear androgen receptor levels are increased after exposure to combined treatment with estradiol benzoate (EB) and dihydrotestosterone (DHT). Thus, adult male rats were castrated and treated for 1 week with either vehicle (0.1 ml sesame oil, s.c), EB (2 µg/day), testosterone (3-cm Silastic implant), DHT (3-cm Silastic implant) or EB + DHT. These treatments produced hormone levels in the physiologic range. We found that both testosterone and DHT significantly stimulated AA (p < 0.05 vs. castrated rats). However, testosterone induced AA significantly more than DHT in the POA (p < 0.05; castrated + testosterone vs. castrated + DHT). EB alone did not affect AA but synergized with DHT to stimulate AA in the POA to levels equivalent with the testosterone-treated group. By comparison, EB alone did not enhance the induction of AA by DHT in the hypothalamus. Combined treatment with EB and DHT had no effect on the concentrations of nuclear androgen receptors in either tissue suggesting that the effect of EB was not mediated through an androgen receptor mechanism. These results suggest that both androgens and estrogens play a physiologic role in the control of estrogen formation in the rat brain. Furthermore, the anatomical specificity that we observed indicates that critical differences in enzyme responsiveness are present in different areas of the brain.
© 1991 S. Karger AG, Basel
Related Articles:
Article / Publication Details
Received: April 17, 1990
Accepted: June 22, 1990
Published online: April 04, 2008
Issue release date: 1991
Number of Print Pages: 6
Number of Figures: 0
Number of Tables: 0
ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)
For additional information: https://www.karger.com/NEN
Copyright / Drug Dosage / Disclaimer
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

Get Permission