A Role for Hypothalamic Astrocytes in Dehydroepiandrosterone and Estradiol Regulation of Gonadotropin-Releasing Hormone (GnRH) Release by GnRH Neurons

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Molecules of astrocyte origin influence gonadotropin-releasing hormone (GnRH) release and GnRH neuronal growth and differentiation. Furthermore, type 1 astrocytes express steroid receptors, presenting the possibility that steroid actions on GnRH neurons might occur via astrocytes. Utilizing GT1–7 cells, a GnRH-secreting cell line, the present study demonstrates that astrocytes mediate dehydroepiandrosterone (DHEA) or estradiol (E2) stimulated GnRH secretion. Conditioned media (CM) from astrocytes cultured for 48 h alone, with DHEA (DHEA-CM), or with E2 (E2-CM) were collected, treated with charcoal to remove steroids, and added to GT1–7 cells in culture for 12 h to test the effect on GnRH secretion. DHEA-CM and E2-CM stimulated GnRH secretion by GT1–7 cells by 4- and 3-fold, respectively. The effect of DHEA-CM on GnRH secretion by GT1–7 cells appears to be related to both DHEA and its metabolite, E2, since blocking the metabolism of DHEA into estrogen in the DHEA-treated astrocytes partially reversed the stimulatory effect of DHEA-CM. Addition of transforming growth factor (TGF)-β1-neutralizing antibody to the astrocyte cultures reversed the stimulatory effects of both DHEA-CM and E2-CM on GnRH secretion by GT1–7 cells, suggesting that TGF-β1 derived from astrocytes may be the principle mediator of E2 and DHEA effects. These data provide evidence for a novel mechanism by which circulating steroids and/or neurosteroids may modulate GnRH secretion.

Related collections

Most cited references 7

Record: found
Abstract: not found
Article: not found

Differential Ligand Activation of Estrogen Receptors ER and ER at AP1 Sites

K Paech (1997)

0 comments Cited 109 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Gonadal hormones as promoters of structural synaptic plasticity: cellular mechanisms.

L.M. Garcia-Segura, J.A. Chowen, A Parducz … (1994)

It is now obvious that the CNS is capable of undergoing a variety of plastic changes at all stages of development. Although the magnitude and distribution of these changes may be more dramatic in the immature animal, the adult brain retains a remarkable capacity for undergoing morphological and functional modifications. Throughout development, as well as in the postpubertal animal, gonadal steroids exert an important influence over the architecture of specific sex steroid-responsive areas, resulting in sexual dimorphisms at both morphological and physiological levels. We are only now beginning to gain insight into the mechanisms involved in gonadal steroid-induced synaptic changes. The number of synaptic inputs to specific neuronal populations is sexually dimorphic and this can be modulated by changes in the sex steroid environment. These modifications can be correlated with other morphological changes, such as glial cell activation, that are occurring simultaneously in the same anatomical area. Indeed, the close physical relationship between glial cells and neuronal synaptic contacts makes them an ideal candidate for participating in this process. Interestingly, not only can the morphology and immunoreactivity of glial cells be modulated by gonadal steroids, but a close negative correlation between the number of synapses and the amount of glial ensheathing of a neuron has been demonstrated, suggesting an active participation of these cells in this process. Glia have sex steroid receptors, are capable of producing and metabolizing steroids, and can produce other neuronal trophic factors in response to sex steroids. Hence, their role in gonadal steroid-induced synaptic plasticity is becoming more apparent. In addition, there is recent evidence that this process may involve certain cell surface molecules, such as the N-CAMs, since a specific isoform of this molecule, previously referred to as the embryonic form, is found in those areas of the brain which maintain the capacity to undergo synaptic remodelling. However, there is much work to be done in order to fully understand this phenomenon and before bringing it into a clinical setting in hopes of treating neurodegenerative diseases or injuries to the nervous system.

0 comments Cited 15 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Absence of androgen receptors in LHRH immunoreactive neurons.

Xiaoping Huang, Richard E Harlan (1993)

Androgen has a negative feedback effect upon reproductive functions. Studies have suggested that this effect is mediated partially at the hypothalamic level. However, it is not clear whether the action is direct or indirect on LHRH neurons. In the present study, double immunocytochemistry was used to localize LHRH and androgen receptors. Out of 5892 LHRH immunoreactive neurons, no double-labelled neurons were observed. We conclude that the feedback effect of androgen on the central nervous system is mediated by indirect pathway(s).

0 comments Cited 13 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (publisher-id): NEN

Journal ID (nlm-ta): Neuroendocrinology

Journal ID (doi): 10.1159/issn.0028-3835

Title: Neuroendocrinology

Publisher: S. Karger AG

ISSN (Print): 0028-3835

ISSN (Electronic): 1423-0194

Publication date Subscription-year: 2002

Publication date (Print): June 2002

Publication date (Electronic): 07 June 2002

Volume: 75

Issue: 6

Pages: 375-383

Affiliations

Department of Reproductive Medicine, University of California, San Diego, La Jolla, Calif., USA

Article

Publisher ID: 59434 Other ID: Neuroendocrinology 2002;75:375–383

DOI: 10.1159/000059434

PubMed ID: 12065890

SO-VID: 085c2a82-ef9f-4c57-b13a-1830c6f0ce25

License:

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.

A Role for Hypothalamic Astrocytes in Dehydroepiandrosterone and Estradiol Regulation of Gonadotropin-Releasing Hormone (GnRH) Release by GnRH Neurons

Read this article at

Abstract

Related collections

Karger: Endocrinology

Most cited references 7

Differential Ligand Activation of Estrogen Receptors ER and ER at AP1 Sites

Gonadal hormones as promoters of structural synaptic plasticity: cellular mechanisms.

Absence of androgen receptors in LHRH immunoreactive neurons.

Author and article information

Journal

Affiliations

Article

History

Page count

Categories

Comments

Comment on this article

Similar content 222

Cited by 5

Most referenced authors 64