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Evidence for a Role of Testosterone-Androgen Receptor Interactions in Mediating Masculine Sexual Behavior in Male Rats^*

Department of Anatomy, Mount Sinai School of Medicine, City University of New York New York, New York 10029

Address all correspondence and requests for reprints to: Dr. Marilyn Y. McGinnis, Department of Anatomy, Mount Sinai School of Medicine, City Uuniversity of New York, 1 Gustave L. Levy Place, New York, New York 10029.

Abstract

The purpose of this study was 2-fold: 1) to use gonadal steroid hormone exposures in the physiological range to assess the relative roles of testosterone (T), estradiol (E₂), and dihydrotestosterone (DHT) in the expression of male sexual behavior, and 2) to determine whether androgen receptor (AR) or estrogen receptor (E₂R) occupation is increased after exposure to these various gonadal steroid hormones. Sexually experienced, castrated male rats implanted sc with Silastic capsules containing T, 10% E₂, DHT, 10% E₂ plus DHT, or blanks provided hormone levels in the physiological range. Copulatory behavior was measured on days 2–4, 5–7, 10–12, and 14–16 of steroid treatment. Although T, E₂, and E₂ plus DHT treatments all activated mounting, only T was effective in restoring ejaculation in 100% of the males. DHT alone had no effect on any aspect of male sexual behavior. Brains of males given these various hormone treatments were assayed for both cell nuclear AR and cell nuclear E₂R binding in the hypothalamus, preoptic area, amygdala, and septum. Results indicate that when hormone levels in the physiological range were employed, T and DHT bind primarily to AR, whereas E₂ binds to E₂R. In a second experiment, 0.5% E₂ plus DHT was found to yield AR and E₂R levels comparable to those in rats receiving T capsules. Male rats bearing these capsules showed virtually no sexual behavior, demonstrating that elevation of AR and E₂R levels comparable to those generated by T is not sufficient to induce male sexual behavior. We then measured intact AR and E₂R levels and determined that in intact males E₂R levels were higher than in T-treated males. These E₂R levels could be replicated using 1.0% E₂. Males exposed to 1.0% E₂ plus DHT failed to display male sexual behavior. These data suggest that 1) relatively high and prolonged levels of E₂R occupation are required for estrogen activation of male sexual behavior, 2) high levels of AR occupation induced by DHT are not sufficient to activate male sexual behavior, and 3) in intact male rats T, acting via androgen receptors, plays a primary role in mediating the expression of masculine sexual behavior. (Endocrinology 124: 618–626,1989)

Footnotes

^* This work was supported by NSF Grant BNS-8312685 (to M.Y.M.) and NIH Summer Fellowship AM-742004 (to R.M.D.).

Received July 15, 1988.

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