title: Immature rats show ovulatory defects similar to those in adult rats lacking prostaglandin and progesterone actions.
abstract: Gonadotropin-primed immature rats (GPIR) constitute a widely used model for the study of ovulation. Although the equivalence between the ovulatory process in immature and adult rats is generally assumed, the morphological and functional characteristics of ovulation in immature rats have been scarcely considered. We describe herein the morphological aspects of the ovulatory process in GPIR and their response to classical ovulation inhibitors, such as the inhibitor of prostaglandin (PG) synthesis indomethacin (INDO) and a progesterone (P) receptor (PR) antagonist (RU486). Immature Wistar rats were primed with equine chorionic gonadotropin (eCG) at 21, 23 or 25 days of age, injected with human chorionic gonadotropin (hCG) 48 h later, and sacrificed 16 h after hCG treatment, to assess follicle rupture and ovulation. Surprisingly, GPIR showed age-related ovulatory defects close similar to those in adult rats lacking P and PG actions. Rats primed with eCG at 21 or 23 days of age showed abnormally ruptured corpora lutea in which the cumulus-oocyte complex (COC) was trapped or had been released to the ovarian interstitum, invading the ovarian stroma and blood and lymphatic vessels. Supplementation of immature rats with exogenous P and/or PG of the E series did not significantly inhibit abnormal follicle rupture. Otherwise, ovulatory defects were practically absent in rats primed with eCG at 25 days of age. GPIR treated with INDO showed the same ovulatory alterations than vehicle-treated ones, although affecting to a higher proportion of follicles. Blocking P actions with RU486 increased the number of COC trapped inside corpora lutea and decreased ovulation. The presence of ovulatory defects in GPIR, suggests that the capacity of the immature ovary to undergo the coordinate changes leading to effective ovulation is not fully established in Wistar rats primed with eCG before 25 days of age.
authors.affiliation: Department of Cell Biology, Physiology and Immunology, School of Medicine, University of Cordoba, Spain. bc1galuf@uco.es
authors.forename: María
authors.initials: M
authors.lastname: Gaytan
authors.forename: Carmen
authors.initials: C
authors.lastname: Bellido
authors.forename: Concepcion
authors.initials: C
authors.lastname: Morales
authors.forename: Marcelino
authors.initials: M
authors.lastname: Gonzalez-Padilla
authors.forename: Jose E
authors.initials: JE
authors.lastname: Sanchez-Criado
authors.forename: Francisco
authors.initials: F
authors.lastname: Gaytan
mesh_terms: D000367:Age Factors; D000818:Animals; D005260:Female; D006064:Gonadotropins, Equine / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D015735:Mifepristone / Q000494:pharmacology; D006080:Ovarian Follicle / Q000033:anatomy & histology / Q000502:physiology; D010060:Ovulation / Q000187:drug effects / Q000502:physiology*; D011374:Progesterone / Q000172:deficiency* / Q000494:pharmacology / Q000502:physiology; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis / Q000172:deficiency* / Q000494:pharmacology / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D011980:Receptors, Progesterone / Q000037:antagonists & inhibitors
chemical_list: D006064:Gonadotropins, Equine; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011980:Receptors, Progesterone; D015735:Mifepristone; D011374:Progesterone; D007213:Indomethacin