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Absence of androgen receptor in the growth hormone releasing hormone-containing neurones in the rat mediobasal hypothalamus

  • M. Fodor*
  • , C. B. M. Oudejans
  • , H. A. Delemarre-van de Waal
  • *Corresponding author for this work
  • Vrije Universiteit Amsterdam
  • Semmelweis University
  • Amsterdam UMC - Vrije Universiteit Amsterdam

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Growth hormone (GH) secretory patterns are influenced by gonadal steroids, at least in part, through modulation of hypothalamic somatostatin and GH releasing hormone (GHRH) secretion. In the adult male rat, testosterone appears to stimulate somatostatin gene expression by acting directly on androgen receptors in somatostatin neurones. The mechanisms by which gonadal status influences hypothalamic GHRH gene expression is less clear. Gonadectomy reduces GHRH mRNA expression in rats, and this reduction can be prevented by the administration of testosterone or partly by a nonaromatizable androgen. While these observations suggest that androgen receptors mediate the actions of gonadal steroids on GHRH gene expression, they do not provide any information about the location of the androgen receptors involved in this process. To determine whether GHRH neurones themselves express androgen receptors, we double immunolabelled hypothalamic sections from colchicine-pretreated male rats. Although there was an overlap in the anatomical distribution of GHRH and androgen receptor-containing cell bodies, none of the nearly 900 GHRH immunolabelled cells we examined in each mediobasal hypothalamus appeared to contain androgen receptors. These results suggest that GHRH-expressing neurones are not direct targets for androgens and therefore the effects of testosterone on GHRH gene expression must be produced indirectly by some other neural or endocrine intermediary process.
Original languageEnglish
Pages (from-to)724-727
JournalJournal of neuroendocrinology
Volume13
Issue number8
DOIs
Publication statusPublished - 2001
Externally publishedYes

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