October 28, 2002
NEL HOME, Newsletter
Z.KLEIN AWARD for Human Ethology
CONTENTS Vol.23 No.4 Aug 2002
VOL.22, 2001
VOL.21, 2000
VOL.20, 1999
VOL.19, 1998
VOL.18, 1997

including Psychoneuroimmunology, Neuro
Reproductive Medicine, Chronobiology
and Human Ethology
ISSN 0172–780X

NEL Vol.23 No.4, August 2002


Galanin and DHEA regulation of prolactin

2002; 23:325328
pii: NEL230402A05
PMID: 12195234

Free full text online pdf [112 kb]
purchace & print HERE

Dehydroepiandrosterone regulation of prolactin gene expression in the anterior pituitary does not depend on galanin induction
Gerardo G. Piroli 1,2,3, Luciana Pietranera 1,2, Claudia A. Grillo 1,2,3 & Alejandro F. De Nicola 1,2

  1. Laboratorio de Bioquímica Neuroendócrina, Instituto de Biología y Medicina Experimental, UBA-CONICET, Buenos Aires, Argentina.
  2. Departamento de Bioquímica Humana, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
  3. Present address: Laboratory of Neuroendocrinology,
    The Rockefeller University, New York, USA

Key words:
pituitary tumor; estrogen; androgen; Fischer 344 rat; prolactinoma

Submitted: June 18, 2002
Accepted: June 24, 2002


OBJECTIVES: The effects of dehydroepiandrosterone (DHEA) on galanin (GAL) and prolactin (PRL) mRNA expression in the anterior pituitary of Fischer 344 rats were studied, taking in consideration that: (1) DHEA is an androgen with estrogenic activity on pituitary lactotrophs; (2) estrogens induce prolactinomas in Fischer 344 rats; and (3) GAL has been considered the main mediator of estrogen-induced lactotroph proliferation.
DESIGN: Female rats were ovariectomized and used as controls or treated during 2 weeks with DHEA (500 mg/kg/day or 5 mg/kg/day or 50 mg/kg/day) or estradiol (E2, 50 mg/kg/day), as a positive control for pituitary growth and GAL induction. GAL and PRL mRNA expression were studied by in situ hybridization.
RESULTS: Both DHEA and E2 induced PRL mRNA synthesis. However, DHEA neither produced pituitary enlargement nor GAL induction, in contrast to E2.
CONCLUSIONS: Our results shows that GAL is not involved in the estrogenic activity of DHEA on pituitary lactotrophs, and suggest that DHEA effects are exerted directly on the PRL gene or through another mechanism(s) not related to GAL.


DHEA – dehydroepiandrosterone
PRL – prolactin
GAL – galanin
E2 – estradiol
OD – optical density


Estrogens increase prolactin (PRL) expression, synthesis and secretion in the rat [1]. When given chronically, estrogens also induce lactotroph proliferation and pituitary enlargement [2]. These effects are enhanced in the Fischer 344 (F344) rat [3–5], and seem to depend on the expression of the peptide galanin (GAL), which is positively regulated by estrogens [4, 6–8]. While GAL is present at very low levels only in somatotrophs in the ovariectomized rat [9], the increment observed in GAL content after estrogenization is due to its expression in lactotrophs [9, 10]. GAL released by some lactotrophs regulates the function of the same or other lactotrophs in an autocrine/paracrine fashion [6, 11].
The adrenal androgen dehydroepiandrosterone (DHEA) exerts estrogenic actions at the pituitary level. Studies with adenohypophyseal cells showed that DHEA increases PRL cell content and reduces lactotrophs' sensitivity to the inhibitory action of dopamine, through a direct interaction of DHEA with estrogen receptors [12]. In vivo studies showed that DHEA increases PRL mRNA content in pituitaries of intact or gonadectomized rats, and also diminishes tyrosine hydroxylase expression in the arcuate nucleus, thus decreasing the dopaminergic inhibitory input on PRL [13].
The present study was performed to test the hypothesis that DHEA modulates PRL expression through the regulation of the GAL gene, by virtue of its estrogenic activity. In addition, we evaluated the possible tumorigenic action of DHEA on the anterior pituitary of F344 rats.

... ...

Copyright  Neuroendocrinology Letters 2002
All rights reserved. No part may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or ortherwise, without prior written permission from the Editor-in-Chief.