Regulation of inhibin/activin subunits and follistatin mRNA expression in the rat pituitary at early estrus.
In the rat pituitary, activin stimulates whereas inhibin prevents FSH synthesis and secretion. Besides, the activin binding protein follistatin neutralizes the action of activin. The control of the FSH secondary surge at early estrus is not completely understood. To investigate the regulation of the inhibin/activin alpha-, betaA- and betaB-subunits and follistatin mRNA expression in the pituitary during the time of the FSH secondary surge, cyclic rats treated with LHRH antagonist (ANT) and ovine LH (oLH), progesterone (P), the anti-steroid RU486, adrenalectomy (ADX) or ADX plus corticosterone (B), were killed at early estrus. The serum concentrations of FSH were measured and the mRNA levels of the above mentioned transcripts were analysed and quantitated by using RNase protection assays. ANT abolished the FSH secondary surge and increased mRNA for alpha- and betaA-subunits and follistatin, but reduced that for betaB-subunit. Both oLH and P reversed these effects. RU486 blocked the effect of oLH on FSH levels and prevented the reduction in the mRNA for follistatin. ADX in ANT+oLH-treated rats reduced the serum FSH concentrations, enhanced mRNA for betaA- and betaB-subunits and, similar to RU486, blocked the drop in follistatin mRNA. Finally, replacement of B in ADX animals reversed these effects. These results demonstrate that, in the cyclic rat, the preovulatory secretion of LH and the surges of P and B on proestrus regulate the synthesis of inhibin/activin subunits and follistatin mRNA in the rat pituitary at early estrus, probably by reducing inhibin and follistatin and increasing activin. Moreover, these effects of LH, P and B at the pituitary level, together with the decrease in the amount of inhibin coming from the ovary, might be responsible for the occurrence of the FSH secondary surge.
Tébar
M
M
Department of Physiology, Faculty of Medicine, University of Córdoba, Spain. tebar@lumc.nl
de Jong
F H
FH
Sánchez-Criado
J E
JE
D028341:Activins; D000315:Adrenalectomy; D000818:Animals; D003345:Corticosterone / Q000494:pharmacology; D004971:Estrus / Q000097:blood / Q000187:drug effects / Q000502:physiology*; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D038681:Follistatin; D005786:Gene Expression Regulation; D006023:Glycoproteins / Q000235:genetics* / Q000378:metabolism; D006727:Hormone Antagonists / Q000494:pharmacology; D007265:Inhibins / Q000235:genetics* / Q000378:metabolism; D015735:Mifepristone / Q000494:pharmacology; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism*; D021122:Protein Subunits; D015347:RNA Probes / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012260:Ribonucleases / Q000378:metabolism; D015854:Up-Regulation
D038681:Follistatin; D006023:Glycoproteins; D006727:Hormone Antagonists; D021122:Protein Subunits; D015347:RNA Probes; D012333:RNA, Messenger; D028341:Activins; D015735:Mifepristone; D007265:Inhibins; D005640:Follicle Stimulating Hormone; D012260:Ribonucleases; D003345:Corticosterone