The volume of the sexually dimorphic nucleus in the preoptic area (SDN-POA) of the rat brain is severalfold larger in adult male rats than in adult females. This sex difference in brain structure was previously shown to develop under the influence of androgenic and estrogenic hormones during the perinatal period. We tried to clarify the differential role played by androgens and estrogens during development and differentiation of the SDN-POA by treating male and female rats during an extended pre- and postnatal period either with the estrogen antagonist tamoxifen or with the androgen antagonist cyproterone acetate. Treatment with tamoxifen did not alter serum levels of testosterone in male rats during the perinatal period, but it inhibited development and differentiation of the SDN-POA. Pre- and postnatal treatment of male rats with cyproterone acetate resulted in female phenotypic appearance, but it had no influence on differentiation of the SDN-POA. Perinatal treatment of female rats with tamoxifen resulted in permanent anovulatory sterility, but did not influence SDN-POA differentiation. Treatment of female rats with cyproterone acetate had no influence on SDN-POA differentiation or on the capacity to ovulate. Since pre- and postnatal treatment of male rats with cyproterone acetate is known from previous studies to feminize sexual behavior patterns and to retain the mode for cyclic gonadotropin release, and since the same treatment did not influence differentiation of the SDN-POA in the present study, it may be concluded that the SDN-POA is not directly involved in the control of female sexual behavior and in the control of the gonadotropic hormone release pattern. The results further indicate that development and differentiation of the SDN-POA is primarily under estrogenic, not under androgenic control.

Newborn rats received daily subcutaneous treatment with compounds which influence serotoninergic, cholinergic, alpha-adrenergic and beta-adrenergic activity. In adulthood luteinizing hormone (LH) secretion pattern, female sexual behavior, and the volume of the sexually dimorphic nucleus of the preoptic are (SDN-POA) were determined. Postnatal administration of l-tryptophan increased the volume of the SDN-POA significantly when given alone or when given simultaneously with testosterone propionate (TP). Para-chlorophenyl-alanine (pCPA) also increased SDN-POA volume, but did not potentiate the stimulating influence of TP. Clonidine had no effect per se on SDN-POA development, but it significantly potentiated the effect of TP in females. Salbutamol increased SDN-POA volume in females and in males. Postnatal treatment of female rats with the alpha-adrenergic receptor antagonists prazosine and yohimbine or with the nicotin receptor antagonist mecamylamine had permanent potentiating effects on the pattern of LH secretion, whereas postnatal treatment with beta-adrenergic compounds reduced the LH-release response to gonadal steroids in adulthood. Postnatal treatment with clonidin or l-tryptophane inhibited differentiation of the capacity for lordosis behavior. Beta-receptor agonists postnatally had a potentiating effect on the capacity for lordosis behavior in female and male rats. Cholinergic stimulation postnatally inhibited differentiation of the capacity for lordosis behavior in female rats, but prevented the inhibitory effect of postnatal androgenization. There was no correlation between SDN-POA volume and any of the two functional parameters.

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