title: Temporal changes in inhibin, steroid hormones, and steroidogenic enzymes during induced follicular atresia in the hypophysectomized cyclic hamster.
abstract: The time course for loss of ability of Graafian follicles to secrete inhibin and estradiol was investigated during induced follicular atresia. Cyclic hamsters were hypophysectomized on Day 1 (estrus) and injected s.c. with 30 IU eCG. Thereafter, these animals were given a single i.p. injection of antiserum to eCG on the morning of Day 4 to induce follicular atresia in a rapid and predictable manner. A drastic fall in plasma levels of estradiol and testosterone was noted within 1 h, whereas relatively high levels of plasma inhibin were maintained until 12 h, followed by an abrupt decline by 24 h. The first histological signs of pyknosis in granulosa cells appeared by 4 h, and breakdown of the mural granulosa layer was observed in most follicles by 8-12 h after immunoneutralization of circulating eCG. According to immunohistochemical analysis, inhibin activity was unchanged in granulosa cells at 12 h followed by a slight decline by 24 h, whereas positive reaction for aromatase in these cells rapidly declined by 8 h. Immunoreactivity of 17alpha-hydroxylase/C17,20-lyase (CYP 17) was also reduced in theca cells by 8 h. These results indicate that granulosa cells continue to secrete inhibin during the process of follicular atresia, although these cells quickly shut off the secretion of estradiol, and theca cells shut off the secretion of testosterone. The present results indicate as well that a rapid decline of estradiol and testosterone in plasma is an early sign of atresia in antral follicles. These results, therefore, suggest that the loss of enzymatic activity of aromatase in granulosa cells and CYP 17 in theca cells is a part of the process of follicular atresia.
authors.affiliation: Laboratory of Veterinary Physiology, Tokyo University of Agriculture and Technology, Fuchu, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Otsuka
authors.forename: H
authors.initials: H
authors.lastname: Kishi
authors.forename: K
authors.initials: K
authors.lastname: Arai
authors.forename: G
authors.initials: G
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Taya
authors.forename: G S
authors.initials: GS
authors.lastname: Greenwald
mesh_terms: D000818:Animals; D001141:Aromatase / Q000378:metabolism*; D006063:Chorionic Gonadotropin / Q000276:immunology / Q000502:physiology; D006224:Cricetinae; D004958:Estradiol / Q000378:metabolism*; D005260:Female; D005496:Follicular Atresia / Q000502:physiology*; D006107:Granulosa Cells / Q000201:enzymology / Q000378:metabolism; D007016:Hypophysectomy; D007116:Immunization, Passive; D007150:Immunohistochemistry; D007265:Inhibins / Q000378:metabolism*; D007700:Kinetics; D008647:Mesocricetus; D006080:Ovarian Follicle / Q000201:enzymology / Q000502:physiology; D011374:Progesterone / Q000097:blood; D013254:Steroid 17-alpha-Hydroxylase / Q000378:metabolism*; D013739:Testosterone / Q000378:metabolism; D013799:Theca Cells / Q000201:enzymology / Q000378:metabolism
chemical_list: D006063:Chorionic Gonadotropin; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D007265:Inhibins; D001141:Aromatase; D013254:Steroid 17-alpha-Hydroxylase