Direct actions of gonadal steroid hormones on FSH secretion and expression in the infantile female rat.
FSH-beta mRNA is dramatically regulated in the infantile female rat anterior pituitary. Elevated plasma levels of FSH correspond with increased FSH-beta mRNA levels which peak on PND 12. The source of this regulation does not appear to be GnRH, since the administration of a potent GnRH antagonist does not suppress FSH-beta mRNA levels. Consequently, we have examined the effects of the gonadal steroid hormones, estrogen and androgen, on the maintenance of gonadotropin secretion and gene expression both in vivo and in vitro. Androgen and estrogen action was blocked in vivo with the specific receptor antagonists, flutamide (150 microg) and tamoxifen (200 microg). Administration of antagonists during two different three day time-periods of infantile life [postnatal day (PND) 8-11 and PND 11-14] resulted in differing effects on both FSH and LH secretion as well as on FSH-beta and LH-beta mRNA levels. Flutamide and tamoxifen treatment both suppressed FSH secretion at either age examined (p < 0.01). LH secretion was suppressed by both treatments but only at the younger of the two ages (p < 0.01). In contrast to its effects on FSH secretion, tamoxifen suppressed FSH-beta mRNA levels in the later group only. LH-beta mRNA levels were suppressed by tamoxifen, but only in the younger age group (p < 0.05). The direct effects of steroid hormones on infantile pituitary gonadotrophs were examined in vitro by incubating cells with dihydrotestosterone propionate (DHTP; 10(-8) M) or 17beta-estradiol (E; 10(-8) M). Both DHT and E treatment stimulated FSH secretion when measured 48 h later (p < 0.01). There were no effects on LH secretion. FSH-beta mRNA levels were also stimulated by DHT at 48 h (p < 0.01). Estradiol treatment transiently increased FSH-beta mRNA levels at 2 and 6 h following treatment (p < 0.01) but not at 48 h. LH-beta levels were suppressed by DHT treatment (p < 0.05), and E transiently elevated LH-beta mRNA levels at 2 h (p < 0.05). Taken together these studies indicate that gonadotrophs from infantile female rats are capable of responding directly to steroid hormones, and may play a role in the selective stimulation of FSH secretion and expression in vivo.
Wilson
M E
ME
Department of Cell Biology, Neurobiology, and Anatomy, Loyola University, Stritch School of Medicine, Maywood, IL 60153, USA.
Handa
R J
RJ
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D002478:Cells, Cultured; D013196:Dihydrotestosterone / Q000031:analogs & derivatives / Q000494:pharmacology; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D005485:Flutamide / Q000494:pharmacology; D005640:Follicle Stimulating Hormone / Q000097:blood*; D005786:Gene Expression Regulation / Q000187:drug effects*; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D006062:Gonadotropins / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood; D008853:Microscopy; D010902:Pituitary Gland / Q000187:drug effects*; D011247:Pregnancy; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013256:Steroids / Q000494:pharmacology*; D013629:Tamoxifen / Q000494:pharmacology
D012739:Gonadal Steroid Hormones; D006062:Gonadotropins; D012333:RNA, Messenger; D013256:Steroids; D013196:Dihydrotestosterone; D013629:Tamoxifen; D004958:Estradiol; D005485:Flutamide; C030445:dihydrotestosterone propionate; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone