Induction and maintenance of gonadotropin and lactogen receptors in hypoprolactinemic rats.
The effect of 2-bromo-alpha-ergocriptine (BR)-induced hypoprolactinemia on the induction and maintenance of testicular gonadotropin and lactogen receptors was studied in 60-day-old rats after receptor regulation by a gonadotropin-releasing hormone agonist analog [[D-Ser-(tBu)6]des-Gly10-GnRH N-ethylamide (GnRH-A)] and in young animals during sexual maturation. In adult animals, BR treatment delayed the reappearance of LH binding in the testis after GnRH-A injection, but had no effect on the recovery of lactogen binding. BR treatment also inhibited the increase of LH binding that occurred in control animals during the experimental period, but did not affect lactogen binding. Furthermore, BR potentiated the effect of GnRH-A on the decrease of Leydig cell testosterone synthesis observed 2 days later in vitro. Eight days after GnRH-A injection, concomitant BR treatment significantly inhibited the recovery of Leydig cell cAMP production. In peripubertal (25- to 46-day-old) animals, BR diminished the normal rise in testicular LH receptors, but did not affect the increase in lactogen receptors. Serum testosterone levels and other features of pubertal development, such as balano-preputial separation and spermatogenesis, were unaffected by hypoprolactinemia. In neonatal female animals, significant lactogen binding was detected at 3 days of age, whereas hCG binding was not demonstrable until 9 days after birth. These findings indicate that the expression of lactogen receptors precedes that of LH receptors in the developing gonad, and that the increase of LH binding in the testis during pubertal development requires normal circulating PRL levels. In adult animals, hypoprolactinemia potentiates GnRH-A-induced desensitization of steroidogenesis and cAMP formation, as well as LH receptor down-regulation, delaying the recovery of these phenomena. Although decreased serum PRL levels were associated with a marked reduction in testicular LH receptors both during development and in adult life, the absence of changes in lactogen receptors indicates that the latter sites are largely independent of the circulating PRL concentration.
D000818:Animals; D002064:Buserelin; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives* / Q000494:pharmacology; D006728:Hormones / Q000494:pharmacology*; D007700:Kinetics; D007986:Luteinizing Hormone / Q000378:metabolism*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D010053:Ovary / Q000187:drug effects / Q000378:metabolism*; D010928:Placental Lactogen / Q000378:metabolism*; D011388:Prolactin / Q000097:blood*; D051381:Rats; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000378:metabolism*; D011974:Receptors, LH; D018000:Receptors, Peptide; D013737:Testis / Q000378:metabolism*; D013739:Testosterone / Q000096:biosynthesis*
D006728:Hormones; D011956:Receptors, Cell Surface; D011974:Receptors, LH; D018000:Receptors, Peptide; C028202:placental lactogen receptor; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D011388:Prolactin; D007986:Luteinizing Hormone; D010928:Placental Lactogen; D002064:Buserelin