Alterations of Ovarian Steroidogenesis Induced by Ovulatory Delay in Immature Rats Treated with Pregnant Mare Serum Gonadotropin1
- 1 February 1982
- journal article
- research article
- Published by Oxford University Press (OUP) in Biology of Reproduction
- Vol. 26 (1) , 129-139
- https://doi.org/10.1095/biolreprod26.1.129
Abstract
Immature rats were maintained on a 14 h of light:10 h of dark schedule (lights on 0600 h). Pregnant mare serum gonadotropin (PMSG, 10 IU) was injected s.c. on day 28 of age to initiate follicular development for subsequent ovulation of .apprx. 10 ova. Phenobarbital (PB) (6.5 mg/100 g body wt) was injected s.c. at 1300 h to induce 1 day of ovulatory delay. Rats treated with 6.5 mg PB on proestrus and 13 mg PB on day 31 at 1200 h exhibited 2 days of delay; additional injections of 19.5 mg and 26 mg PB were required on the next successive days at 1200 h for 3 and 4 days of ovulatory delay, respectively. During the period of delay, serum concentrations of P [progesterone] remained unchanged; serum A [androstanedione] and E2 [estradiol] levels decreased significantly. Atresia of the preovulatory follicles was evident in most animals after 4 days of delay. In the remaining experiments, PMSG from another source was used to initiate follicular development for subsequent ovulation of .apprx. 10 ova. Serum E2 levels on the morning of day 2 of delay were significantly higher than those levels in rats receiving PMSG (from the first source) although serum A levels declined and P levels remained unchanged. In vitro ovarian steroidogenesis revealed that the ovaries of rats with a delayed ovulation produced more P and less A than controls in response to 1 .mu.g LH [lutropin] (ovine S22) in vitro. Although 1 .mu.g LH in vitro did not induce E2 secretion, ovaries of PB-treated rats produced more E2 than those of nondelayed controls. During the LH/FSH surge (1900 h proestrus), serum P levels increased in groups with 0 and 2 days of ovulatory delay; serum A failed to increase after 2 days of delayed ovulation and serum E2 declined. In controls, E2 levels in sera remained unchanged. In vitro ovarian steroidogenesis substantiated the alterations in serum steroids. During 2 days of delayed ovulation, 25 .mu.l equine antibovine LH (anti-LH) administered on day 30 induced a decline in serum E2 without alteration of serum P and A. Anti-LH (25 .mu.l) given on each day of delay lowered the serum level of A and E2 but not P; 100 .mu.l anti-LH administered on each day of delay lowered serum concentrations of P, A and E2. Ergocryptine (400 .mu.g CB-154) given on days 30 and 31 lowered serum prolactin concentrations and partially prevented the decline in serum A levels without alteration of serum P and E2. The PMSG-treated immature rat is a useful model for the study of atresia, ovulatory delay inhibits ovarian A secretion (and E2, but this depends on the type of PMSG); prolactin may be causally related to the alteration in A synthesis and preovulatory follicles are sensitive to gonadotropin deprivation during ovulatory delay.This publication has 14 references indexed in Scilit:
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