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The Regulation of Oxytocin Receptor Binding in the Ventromedial Hypothalaimic Nucleus by Testosterone and Its Metabolites^*

Section on Comparative Studies of Brain and Behavior, Laboratory of Clinical Sciences, National Institute of Mental Health (A.E.J., T.R.I.) Poolesville, Maryland 20837
The Laboratory of Neuroendocrinology, Rockefeller University (H.C., B.S.M.) New York, New York 10021

Address all correspondence and requests for reprints to: Dr. Allan E. Johnson, Department of Pathology, Karolinska Institute, Huddinge Hospital, S-14186 Huddinge, Sweden.

Abstract

Oxytocin (OT) receptor binding in the ventromedial hypothalamic nucleus is regulated by testosterone (T) in male rats. However, T is metabolized in the brain, and many of the central effects of T are mediated by its metabolites. The experiments reported here were designed to determine whether T affects OT receptor binding directly or through the action of its metabolites 17β-estradiol and 5-dihydrotestosterone. Adult male rats were either sham operated or castrated and treated 1 week later with T propionate (TP), 17β-estradiol benzoate (EB), dihydrotestosterone benzoate (DHTB), DHTB plus EB, or oil. OT receptor binding was assessed autoradiographically using [¹²⁸I]d(CH₂)₅[Tyr(Me)²,Thr⁴,Tyr-NH2⁹]OVT. In addition, seminal vesicle weights were measured as an index of androgenic activity. These experiments showed that TP and DHTB plus EB increased OT receptor binding in the ventromedial hypothalamic nucleus to the levels in intact males. Treatment with EB alone partially reinstated binding to the levels in intact males, while DHTB treatment was without effect. Castrated males treated with either TP or DHTB had seminal vesicle weights comparable to those of gonadally intact males and greater than those of animals in all other steroid conditions, indicating that sufficient levels of circulating steroids were attained in these groups. These data suggest that the induction of hypothalamic OT receptor binding by T is the result of the combined actions of estradiol and dihydrotestosterone. However, the mechanism underlying this interaction is unknown. (Endocrinology 128: 891–896,1991)

Footnotes

^* This work was supported in part by grants from the Consejo Nacional de Investigaciones Cientificas y Tecnicas de la Republica Argentina (to H.C.) and Grant NS-07080 (to B.S.M.).

Received July 16, 1990.

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