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Regulation of Pituitary Follistatin and Inhibin/Activin Subunit Messenger Ribonucleic Acids (mRNAs) in Male and Female Rats: Evidence for Inhibin Regulation of Follistatin mRNA in Females¹

Division of Endocrinology, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908

Address all correspondence and requests for reprints to: Dr. A. C. Dalkin, Division of Endocrinology, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908. E-mail: acd6v{at}virginia.edu

The regulation of FSHß messenger RNA (mRNA) expression is complex and involves signals from the hypothalamus and gonads. Additionally, the local (pituitary) production of activin and follistatin appears to serve as an important modulator of endocrine signals for FSHß regulation. The purpose of these studies was to identify factors controlling pituitary activin/inhibin subunit and follistatin mRNA production in male and female rats. Both males and females expressed the follistatin, inhibin , and ßB mRNAs, whereas the ßA mRNA was not detected. In males, levels of FSHß and follistatin were higher than those in females. After gonadectomy, levels of FSHß and follistatin increased in both sexes, whereas ßB rose only in females. In males, blockade of GnRH action from the time of castration prevented the increase in FSHß and follistatin, suggesting that GnRH is the primary stimulus for these gene products. In females, treatment with a GnRH antagonist only partially prevented the rise in FSHß, follistatin, and ßB expression, suggesting that other factors were also important. Passive immunoneutralization of circulating inhibin increased FSHß and follistatin (but not ßB), providing evidence that inhibin is a physiological regulator of follistatin. Replacement of estradiol at the time of ovariectomy prevented the increase in ßB mRNA, suggesting that gonadal steroids may also act via local factors to regulate FSHß. In summary, these studies provide evidence that GnRH, gonadal steroids, and gonadal peptides probably regulate FSHß expression at least in part via the intrapituitary activin/follistatin system.

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