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Dexamethasone Alters Responses of Pituitary Gonadotropin-Releasing Hormone (GnRH) Receptors, Gonadotropin Subunit Messenger Ribonucleic Acids, and Gonadotropins to Pulsatile GnRH in Male Rats^*

Division of Endocrinology and Metabolism, Department of Internal Medicine, Veterans Administration Medical Center, University of Michigan Ann Arbor, Michigan 48105

Abstract

Dexamethasone (Dex), when administered in high doses, has been shown to suppress spontaneous and GnRHinduced gonadotropin secretion, but the level and the mechanism( s) of this effect are unknown. We administered Dex to castrate testosterone-replaced male rats to determine if gonadotropin gene expression is affected and whether Dex differentially influences GnRH-modulated parameters of gonadotrope function: induction of GnRH receptors (GnRH-R) and gonadotropin synthesis and secretion. GnRH was given iv at 25 ng/ pulse at 8, 30, and 120 min intervals for 48 h. Rapid GnRH injection frequency preferentially increased and LH-β messenger RNA (mRNA) responses to GnRH as well as LH secretion. Slower GnRH injection frequencies were required to increase levels of GnRH-R, FSH-β mRNA, and FSH secretion. Dex selectively inhibited the serum LH, a, and LH-β mRNA responses to GnRH, but not the serum FSH or FSH-β mRNA responses. Additionally, it augmented the GnRH-induced increase in GnRH-R. We conclude: 1) induction of GnRH-R, gonadotropin synthesis, and secretion require different modes of GnRH stimulation; 2) Dex acts directly on the gonadotrope to differentially modulate GnRH-induced increases in GnRH-R levels, gonadotropin gene expression, and gonadotropin secretion; and 3) GnRH effects upon induction of GnRH-R, LH, and FSH synthesis and secretion are likely to be mediated via different cellular pathways. (Endocrinology 128: 654–660,1991)

Footnotes

^* This work was supported by the VA Research Service and by NIH Grant R-29 DK-38449 (to A.B.).

Received August 30, 1990.

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