POSSIBLE MODULA TI ON OF PROLACTIN SECRETION BY TESTOSTERONE IN THE MALE RHESUS MONKEY

Abstract

The present study was undertaken to systematically examine the effect of a neuroexcitatory amino acid , N-methyl-DL-aspartate (NMA ), on plasma PRL release in orchidectomized rhesus monkeys in the absence and in presence of testicular steroidal environment. In the initial experiment PRL response to a single iv injection of NMA was assessed in intact and orchidectomized rhesus monkeys. Blood samples were obtained 50 min before and 70 min following the NMA injection (1 5 mg/kg BW) at 10 min intervals through a teflon cannula implanted in the saphenous vein. All bleedings were carried out under ketamine hydrochloride anaesthesia (initial dose 5 mg/kg followed by 2.5 mg/kg BW at 30 min intervals) . In the second experiment, three chronically orchidectomi z ed rhesus monkeys were given testosterone enanthate in oil (im) in a dose of 250 mg/week for 1 month. Using an identical blood sampling regimen PRL responsiveness to NMA was studied at 0, 1, 2 and 4 weeks following testosterone treatment. The plasma levels of PRL, testosterone and oestradiol were determined by specific radioimmunoassays. In intact monkeys, plasma PRL concentrations rose rapidly following NMA administration. No significant increase in plasma PRL level ' was noticed in orchidectomized rhesus monkeys treated identically with NMA. Administration of testosterone enanthate for a period of 4 weeks to castrated monkeys resulted in a progressive increase in mean plasma PRL concentrations and the levels were 2.2-fold greater at the end of the fourth week of treatment compared to levels determined at the start of the experiment. II The PRL response to NMA challenge was insignificant at 0 and 1 week following testosterone replacement. However, a detectable increase in PRL responsiveness to the neuroexcitatory amino acid was observed in the second week of treatment and a several-fold increase in plasma PRL concentrations were observed in response to the NMA administration during the fourth wee k of testosterone treatment. The present data indicate that NMA dependent release of PRL is modulated by testicular secretions and that administration of testosterone to castrated monkeys not only enhances the PRL secretion but also restores the PRL response to the exogenously administered aspartate agonist. Whether the observed influence of testosterone on NMA induced PRL release is an androgenic effect or that the effect is mediated by a metabolite of testosterone (e.g oestradiol) has yet to be ascertained.