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Androgen Receptors in Gonadotrophs in Pituitary Cultures from Adult Male Monkeys and Rats

Division of Endocrinology and Metabolism, University of Louisville, Louisville, Kentucky 40202

Address all correspondence and requests for reprints to: Stephen J. Winters, M.D., Division of Endocrinology and Metabolism, University of Louisville Health Sciences Center, ACB-A3G11, 530 South Jackson Street, Louisville, Kentucky 40202. E-mail: sjwint01{at}louisville.edu.

There is substantial evidence demonstrating that the principal feedback action of androgens to decrease LH secretion in male primates, including man, is to slow the GnRH pulse generator, whereas in male rats androgens not only decrease GnRH but also suppress LH synthesis and secretion through a direct pituitary effect. Previous experiments in our laboratory revealed that testosterone (T) suppresses LH secretion and decreases -subunit mRNA levels in male rat pituitary cell cultures perifused with pulses of GnRH but not in pituitary cells from adult male monkeys. In the present study, we sought to determine whether the lack of responsiveness of gonadotrophs to androgens in the primate is androgen receptor (AR) related. Primary cultures were prepared from the anterior pituitary glands of adult male monkeys and rats. Cells were identified as gonadotrophs if they were immunoreactive for LH-ß or FSH-ß. Of these cells in the monkey, 80% contained both gonadotropins, 17% contained only LH-ß, and 3% contained only FSH-ß. AR immunoreactivity (IR) was nuclear in 22% and 15%, respectively, of monkey and rat FSH-ß-positive cells in the absence of T. Following T treatment, nuclear AR IR was identified in 79% of monkey and 81% of rat gonadotrophs. T treatment similarly intensified AR IR in mouse gonadotroph T3-1 and LßT2 cells and in monkey and rat fibroblasts. Single-cell RT-PCR confirmed coexpression of LH-ß and AR mRNA as well as LH-ß and GH mRNA in monkey gonadotrophs. Our data reveal that most monkey, as well as rat, gonadotrophs are AR-positive with nuclear localization in the presence of T. GH expression is not required for AR expression in gonadotrophs. We conclude that the failure of T to inhibit LH secretion and decrease -subunit mRNA expression in the male primate is not due a disturbance in AR nuclear shuttling.

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