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Gonadotropin-Releasing Hormone Regulates Follicle- Stimulating Hormone β-Subunit Gene Expression in the Male Rat

Endocrinology Research Group, Clinical Research Centre Harrow, HA1 3UJ United Kingdom

Address all correspondence and requests for reprints to: Dr. Richard Clayton, Clinical Research Center, Endocrinology Research Group, Watford Road, Harrow, Middlesex, HAl 3UJ United Kingdom.

Abstract

Since the role of GnRH in the control of FSH release and synthesis is controversial, we have examined the effect of elimination of GnRH action on gonadotropes on FSHβ gene expression, FSH release, and synthesis. GnRH stimulation of the pituitary was abolished by continuous infusion of either a GnRH antagonist or a GnRH antiserum. We also examined the effects of gonadotrope desensitization, using a continuous infusion of GnRH or GnRH agonist analog. FSHβ mRNA levels were determined by dot blot hybridization using rat FSHβ cDNA, and changes were related to pituitary and serum FSH concentrations.

FSHβ mRNA levels increased after orchidectomy and correlated well with serum FSH concentrations. Overall FSH synthesis was increased after castration, as judged by elevated serum FSH and unchanged pituitary FSH content. In orchidectomized rats, continuous GnRH antagonist infusion prevented the postcastration rise in FSHβ mRNA levels and serum FSH. Pituitary FSH content was reduced at 7 days, but not at 14 days. In intact rats, GnRH antagonist infusion for 7 days had no effect on FSHβ mRNA levels, but after 14 days, there was a 33% reduction, and serum FSH was suppressed. Pituitary FSH content was decreased after GnRH antagonist treatment for 7 or 14 days. Daily injection of GnRH antiserum for 6 days abolished the increases in FSHβ mRNA levels and serum FSH in orchidectomized rats, but pituitary FSH content was unaffected. In intact rats, GnRH antiserum treatment reduced FSHβ mRNA levels by 38%, suppressed serum FSH, and decreased pituitary FSH content. When gonadotropes were desensitized by a continuous infusion of GnRH for 14 days or GnRH agonist analog for 28 days, FSH/8 mRNA levels and pituitary FSH content were markedly reduced, and serum FSH was suppressed to undetectable levels.

We concluded that 1) endogenous GnRH is required for the maintenance of FSHβ mRNA levels in both intact and orchidectomized rats; 2) FSHβ mRNA levels are coupled to the level of FSH biosynthesis, indicating the physiological importance of this pretranslational regulation; 3) desensitization is more effective at inhibiting FSHβ gene expression and FSH synthesis than preventing gonadotrope stimulation using the GnRH antagonist or antiserum; and 4) the actions of GnRH on FSHβ mRNA levels are paralleled by its effects on LHβ mRNA levels, suggesting that GnRH provides a common primary stimulus for the induction of both β-subunit genes in vivo. These data provide further evidence for the crucial stimulatory role of GnRH in the control of FSH synthesis.

Received March 17, 1989.

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