REGULATION OF PROLACTIN BINDING SITES IN THE SEMINAL VESICLE, PROSTATE GLAND, TESTIS AND LIVER OF INTACT AND CASTRATED ADULT RATS: EFFECT OF ADMINISTRATION OF TESTOSTERONE, 2-BROMO-α-ERGOCRYPTINE AND FLUPHENAZINE

Abstract

The effect of hormonal manipulations on prolactin binding to its specific binding sites in the seminal vesicle, prostate gland, testis and liver of adult male rats was studied. Castration significantly reduced prolactin binding to the seminal vesicle and prostate, whereas it greatly increased its binding to the liver. Testosterone replacement therapy restored the reduced level of binding to that found in the liver of intact rats, whereas binding to the seminal vesicle and the prostate was raised to the high levels found in the testosterone-treated intact rats. In contrast, testosterone administration to intact rats significantly reduced the binding of prolactin to the testicular homogenate. The administration of 2-bromo-α-ergocryptine (CB 154) to either intact or testosterone-treated castrated rats caused no significant change in binding of prolactin to any of the organs tested. Fluphenazine enanthate or CB 154 +ovine prolactin increased the binding of prolactin to the liver, when compared with untreated rats, whereas in the testis these treatments resulted in a minor decrease as compared with untreated rats. In the testosterone-treated castrated rats, fluphenazine caused no apparent effect on the binding of prolactin to any of the organs tested. In conclusion, testosterone is essential for the maintenance of prolactin binding sites in the seminal vesicle and prostate of the adult rat. Prolactin, however, does not appear to regulate its own receptor in the accessory sex glands, neither alone nor in synergism with testosterone. In the testis, exogenous testosterone exerted a negative effect on prolactin binding, as did raised serum prolactin levels. In the liver of the male rat, testosterone seemed to be the major cause of the low level of prolactin binding sites, while prolactin was capable of inducing its own sites in that organ.