ROLE OF GONADAL AND ADRENAL-STEROIDS IN THE IMPAIRMENT OF THE MALE-RATS SEXUAL-BEHAVIOR BY HYPERPROLACTINEMIA

The sexual behavior of male rats, castrated and testosterone-implanted, declined following induction of hyperprolactinemia by domperidone. Treatment with estradiol benzoate did not reverse this effect, and may have accentuated it. Estradiol also amplified domperidone-induced hyperprolactinemia. Testosterone or dihydrotestosterone (DHT) apparently delayed, but did not prevent, the gradual deterioration in sexual behavior (prolonged ejaculation latencies) induced by domperidone, but this effect was not confirmed statistically. Adrenalectomy, followed by cortisol replacement, failed to prevent the behavioral effects of hyperprolactinemia. No consistent changes in serum progesterone or corticosterone could be found in hyperprolactinemic rats in which the adrenals were not removed. In vitro formation of DHT from precursor testosterone was reduced in the amygdalae of hyperprolactinemic rats, but not in the hypothalamus or caudal spinal cord. Estradiol cytosol binding was unchanged in all brain areas, except for a small but significant increase in the anterior hypothalamus. A role for altered adrenal activity in determining the effects of high levels of prolactin on sexual behavior is thus not supported. There is evidence for an impaired formation of DHT in the brain, but this may account for only part of the behavioral changes observed. The major effect of prolactin probably lies in neural systems directly responsive to it, rather than in altered steroid secretion or metabolism.