title: Contribution of endogenous inhibin to the decline of the secondary surge of follicle-stimulating hormone in the rat.
abstract: The involvement of inhibin in the decline of the secondary surge of follicle-stimulating hormone (FSH) was investigated in the rat. After ovariectomy or treatment with inhibin antiserum conducted at 2300 hours during pro-oestrus, plasma concentrations of FSH were maintained at high levels compared with control rats. However, plasma FSH started to decline at 0500 hours during oestrus in both the groups. The same treatments conducted during metoestrus markedly increased plasma FSH after 24 h (twofold compared with the treatments during pro-oestrus), suggesting that the treatments sufficiently depleted circulating inhibin. To examine whether the decline of plasma FSH occurred through a transcriptional mechanism or through a translational mechanism, FSH-beta mRNA expression and the pituitary concentration of FSH were measured. Neither ovariectomy nor inhibin immunization conducted during the night of pro-oestrus, affected the pituitary concentration of FSH after 24 h, whereas a noticeable increase was observed after the treatments conducted during metoestrus. In both stages, both ovariectomy and inhibin immunization significantly increased FSH-beta mRNA expression compared with control rats. In contrast with the pituitary concentration of FSH, the effect of inhibin immunization on FSH-beta mRNA expression was not different between the stages. The present data demonstrate the involvement of inhibin in the decline of the secondary surge of FSH, and suggest that a factor or factors other than inhibin may also be responsible for the fall in FSH. Changes in the pituitary concentration of FSH and FSH-beta mRNA expression suggest that post-transcriptional mechanisms may be involved in the suppression of FSH secretion during oestrus.
authors.affiliation: Department of Tissue Physiology, Faculty of Agriculture, Tokyo University of Agriculture and Technology, Fuchu, Japan. kojiarai@cc.tuat.ac.jp
authors.forename: K Y
authors.initials: KY
authors.lastname: Arai
authors.forename: G
authors.initials: G
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Arai
authors.forename: K
authors.initials: K
authors.lastname: Uehara
authors.forename: K
authors.initials: K
authors.lastname: Taya
mesh_terms: D000818:Animals; D005260:Female; D005640:Follicle Stimulating Hormone / Q000032:analysis / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D037201:Follicle Stimulating Hormone, beta Subunit; D015870:Gene Expression; D007106:Immune Sera / Q000494:pharmacology; D007116:Immunization, Passive; D007265:Inhibins / Q000276:immunology / Q000502:physiology*; D007986:Luteinizing Hormone / Q000032:analysis / Q000235:genetics; D008686:Metestrus; D010052:Ovariectomy; D010902:Pituitary Gland / Q000737:chemistry; D011359:Proestrus; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar
chemical_list: D037201:Follicle Stimulating Hormone, beta Subunit; D007106:Immune Sera; D012333:RNA, Messenger; D007265:Inhibins; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone