Gonadal regulation of pituitary gonadotropin-releasing hormone receptors during sexual maturation in the rat.

The number of pituitary GnRH receptors increases during sexual maturation in rats. In females, GnRH receptor content (GnRH-RC, femtomoles bound per gland) rises to a plateau (50 +/- 9 fmol) between 15-30 days of age before increasing further to 107 +/- 19 at 50 days. In males, GnRH-RC rises gradually to 140 +/- 9 fmol at 35 days, then remains stable through 60 days. Administration of estradiol or testosterone to immature females and males, respectively, inhibits the early rise in GnRH-RC. GnRH given for 2 days to steroid-treated immature animals restores receptor content to control levels. Neonatal castration in both sexes rapidly increases GnRH-RC and this response is maintained through 60 days of age. Castrations performed at different ages between 5-60 days showed a sex difference in GnRH-RC responses. Females exhibited a 2-fold increase in GnRH-RC by 5 days post castration at all ages studied. In males a similar increase in GnRH-RC was seen up to 25 days, but later diminished and no receptor response occurred when castration was performed between 30-45 days of age. Orchidectomy after 50 days again resulted in a 2-fold rise in GnRH-RC. GnRH injections (20 micrograms/day in divided doses) increased GnRH-RC in intact males at all ages studied. The same dosage did not increase GnRH receptors in 35-45 day male castrates and 5- to 10-fold higher doses were required to increase GnRH-RC indicating reduced receptor responsiveness to GnRH. Serum gonadotropins increased in response to castration at all ages in both sexes and did not parallel receptor responses in males. These data indicate that pituitary GnRH receptors are modulated by gonadal steroids from day 10 of life in both sexes and that the mechanism involves modification of hypothalamic GnRH secretion. Additionally, factor(s) other than gonadal steroids are operative in males during maturation which alter pituitary receptor responses to GnRH and result in discordant receptor and gonadotropin responses to GnRH.