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