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ABSTRACT
The effect on first ovulation of the massive reduction of the total pool of ovarian follicles during the infantile and late juvenile period was studied in rats. Treatment with an LH-releasing hormone antagonist (LHRH-A) during infancy (5 mg/kg body weight on days 6, 9, 12 and 15 of life) was combined with unilateral ovariectomy performed on either day 15 (early ULO) or 2–5 days before the expected day of first ovulation (late ULO). Rats were killed on the day of first or second oestrus, when blood was collected and the (remaining) ovaries were prepared for differential counting of follicles and corpora lutea. In addition, blood was sampled 8 h after ULO and the ovaries studied histologically in the group of rats which were unilaterally ovariectomized 2–5 days before first ovulation.
The time of first ovulation was not influenced by treatment with LHRH-A, early or late ULO, or a combination of LHRH-A treatment and ULO. Ovulation rate after LHRH-A treatment was decreased, but was still within the normal range in intact rats and in early ULO rats compared with saline-treated controls.
Serum FSH concentrations 8 h after ULO performed 2–5 days before first ovulation were similar in saline- and LHRH-A-treated rats (845 ± 59 and 801 ± 99 (s.e.m.) μg/l respectively) and had increased compared with intact controls (216 ± 15 μg/l).
Treatment with LHRH-A resulted in a reduction of more than 50% in healthy and atretic follicles, and late ULO reduced the number of healthy follicles even further. In saline-treated rats late ULO decreased the rate of atresia, but in LHRH-A-treated rats atresia was not reduced further by (late or early) ULO.
It is concluded that even after massive reduction of the pool of ovarian follicles by early LHRH-A treatment combined with late or early ULO, the timing of the first ovulation was normal and ovulation rates, although somewhat lower in some LHRH-A-treated rats, were within the normal range.
Journal of Endocrinology (1992) 135, 439–446
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ABSTRACT
The possible existence of peripheral asymmetry in the neuroendocrine mechanisms participating in the response of the ovary to gonadotrophins, and the participation of the vagus nerve, was investigated. At oestrus, the ovulation rate (number of ovulating/number of treated rats) of the left ovary in right unilaterally ovariectomized rats was lower than that in the right ovary in left unilaterally ovariectomized rats (42 vs 84%). No differences in the number of ova shed per ovulating animal nor in compensatory ovarian hypertrophy (COH) were observed. Bilateral section of the vagus nerve resulted in reduced COH only in those animals with the left ovary in situ (right unilaterally ovariectomized). Section of the left vagus nerve induced different effects depending upon which ovary was left in situ. When the left ovary was in situ an increase in ovulation rate, COH and number of ova shed was observed; however, when the right ovary was left in place the above three parameters decreased. Section of the right vagus nerve produced a decrease only in COH in both right and left unilaterally ovariectomized animals. It is concluded that in the unilaterally ovariectomized rat the right ovary seems more able to react to compensatory regulatory systems than does the left. The character of the information carried by the left and right vagus nerve is different.
J. Endocr. (1987) 113, 397–401
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ABSTRACT
The gonadotrophic requirements for the induction of ovulation and formation of a viable corpus luteum in two breeds of seasonally anoestrous sheep of differing fecundity was investigated.
Welsh Mountain (n = 20) and Damline ewes (n = 19) were given LH or FSH either alone or in combination. Luteinizing hormone was injected i.v. at an increasing frequency for 72 h (one injection every 3 h for 24 h, one every 2 h for 24 h, and one every hour for 24 h) and FSH was injected in an identical manner for the first 36 h of treatment.
Exogenous LH alone and in combination with FSH induced a preovulatory LH surge in all 19 ewes and ovulation in 18 out of 19 ewes of both breeds. However exogenous FSH alone was ineffective. The incidence of normal corpus luteum function in ewes induced to ovulate was low and not related to treatment, timing or magnitude of the LH/FSH surge. It is concluded that in both breeds studied (a) it is the infrequency of LH pulses which limits the development of preovulatory follicles during seasonal anoestrus, (b) that the requirement for FSH remains unknown, and (c) that the induction of inadequate corpora lutea during seasonal anoestrus reflects either defects in hormonal priming of the preovulatory follicle and/or inappropriate luteotrophic support after ovulation.
J. Endocr. (1986) 111, 181–190
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A selective surge of FSH with a small concomitant rise in LH occurred invariably in rats when ovulation was induced by injecting human chorionic gonadotrophin (HCG) at various reproductive stages such as day 15 of lactation and in 29-day-old immature rats as well as in dioestrous animals. No FSH surge occurred on day 3 of lactation or in 26-day-old immature rats in which ovulation could not be induced by HCG. The FSH surge occurred 6–18 h after HCG treatment regardless of the time of day of injection of HCG. Ovulation began by 12 h and was completed by 18 h after injection of HCG.
Pituitary responsiveness to luteinizing hormone releasing hormone (LH-RH) with respect to FSH release strikingly increased at 01.00 h on day 1 after HCG injection at 17.00 h of dioestrus (day 0) to levels similar to those of the group at 01.00 h of oestrus, when the greatest response was noted during the normal cycle. With regard to LH release pituitary responsiveness to LH-RH at 01·00 h on day 1 markedly increased but the response was only about half of the response at 01·00 h of oestrus and one third of the response at 17.00 h of pro-oestrus when the greatest response was noted during the normal oestrous cycle.
These results indicate that during ovulation the pituitary gland of the rat is highly responsive to LH-RH with respect to the release of FSH, for which secretory changes in the ovary after an ovulating dose of HCG may be responsible.
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The ovulatory process in mammals involves gross physiological events in the ovary that cause transient deterioration of the ovarian connective tissue and rupture of the apical walls of mature follicles. This gonadotropin-induced process has features similar to an acute inflammatory reaction that affects most of the ovary. The present study reveals that the ovulatory events include induction of mRNA for pancreatitis-associated protein-III (PAP-III). Immature Wistar rats were primed with 10 IU equine chorionic gonadotropin s.c., and 48 h later the 12-h ovulatory process was initiated by 10 IU human chorionic gonadotropin (hCG) s.c. Ovarian RNA was extracted at 0, 2, 4, 8, 12 and 24 h after the animals were injected with hCG. The RNA extracts were used for RT-PCR differential display to detect PAP-III gene expression in the stimulated ovarian tissue. Northern blotting showed that transcription was significantly greater at 4-12 h after the ovaries had been stimulated by hCG. In situ hybridization indicated that PAP-III mRNA expression was limited mainly to the hilar region of the ovarian stroma, with most of the signal emanating from endothelial cells that lined the inner walls of blood vessels, and from small secondary follicles. Treatment of the animals with ovulation-blocking doses of indomethacin (an inhibitor of prostanoid synthesis) or epostane (an inhibitor of progesterone synthesis) revealed that ovarian transcription of PAP-III mRNA was moderately dependent on ovarian progesterone synthesis. In conclusion, the present evidence of an increase in PAP-III gene expression in gonadotropin-stimulated ovaries provides further evidence that the ovulatory process is comparable to an inflammatory reaction.
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SUMMARY
Concentrations of cyclic AMP were measured in rabbit ovaries at various times after injection of an ovulatory dose of human chorionic gonadotrophin (HCG). A biphasic increase in cyclic AMP concentration occurred during the preovulatory period, with peaks 30 min and 3–4 h after HCG injection. Concentrations of cyclic AMP had returned to those observed in ovaries of control oestrous animals before the onset of ovulation 10–12 h after administration of HCG, and remained low throughout the period of pseudopregnancy. Concentrations of cyclic AMP in the newly formed and developing corpora lutea were similar to the concentrations observed in the remainder of the tissue during this period. No significant increase in cyclic AMP concentration was observed 7–9 days after initiation of ovulation. Concentrations of ATP were also investigated during the preovulatory period. The dose– response relationship of HCG to cyclic AMP production in oestrous rabbit ovaries was investigated.
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When bovine follicular fluid (BFF) was given i.p. three times at intervals of 3 h from 17.00 to 23.00 h to dioestrous rats pretreated with 10 i.u. human chorionic gonadotrophin (HCG) at 17.00 h on the day of dioestrus (day 0), the selective surge of FSH at 02.00 h on day 1 was suppressed in a dose-dependent manner. Three i.p. injections of 0·5 ml BFF completely suppressed the FSH rise in plasma at 02.00 h on day 1, but the time of premature ovulation induced by HCG was not altered. In these animals treated with HCG and BFF, however, the selective surge of FSH occurred as a delayed surge from 05.00 to 23.00 h on day 1. After seven i.p. injections of 0·5 ml BFF (from 17.00 h on day 0 to 11.00 h on day 1) the delayed surge of FSH took place from 17.00 h on day 1 to 11.00 h on day 2, indicating that waning of BFF with a decrease in inhibin secretion by the ovaries may be responsible for the delay of the FSH surge.
The next spontaneous ovulation in rats treated with HCG and BFF occurred on day 5, a delay of ovulation of 1 day compared with animals given HCG on day 0 with no BFF. Initiation of follicular maturation or selection of growing follicles for the succeeding oestrous cycle appeared to be retarded by the delay of the FSH surge in HCG- and BFF-treated animals.
The pituitary content of FSH in animals given HCG and three i.p. injections of 0·5 ml BFF increased strikingly until 11.00 h on day 1, when the delayed FSH surge was already in progress. These results suggest that the ability of the pituitary gland to synthesize FSH is high during the period of ovulation.
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SUMMARY
Fifty-five mature oestrous does were injected intravenously with luteinizing hormone (LH) and subsequently killed between 9 hr. 52 min. and 14 hr. 30 min. after injection. At autopsy the number of freshly ruptured follicles was counted and was expressed as a percentage of the total number of follicles (ruptured and unruptured) counted, that had undergone pre-ovulatory swelling. This method of calculating 'percentage ovulation' gave results which agreed very closely with previously reported data. The calculation showed no ovulation by 10 hr., 50% ovulation between 10½ and 10¾ hr., and 100% ovulation by 14 hr. after the injection of LH.
In thirty-nine out of these fifty-five does a special study was carried out to determine in what position (in the ruptured follicle, on the surface of the ovary or in the Fallopian tube) the eggs from the ruptured follicles were recovered in relation to the time elapsing after LH injection. Between 10½ and 11½ hr. after injection about 17% of the eggs were found either still inside the ruptured follicle, or within the cumulus oophorus protruding from the follicle or adhering to the ovarian surface. However, at 11½–13 hr. after injection only 3·6–5·9% were still in the follicle or on the ovarian surface. From 13 hr. after LH injection all the eggs recovered were found in the Fallopian tube. These results suggest that not all the eggs are ejected from the follicle at the time of rupture, and that some appreciable time may elapse between follicular rupture and entry of eggs into the tube.
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SUMMARY
The majority of rats exposed to constant light for approximately 6 weeks ovulated within 24 hr. after an injection of human chorionic gonadotrophin (HCG), but required 24–48 hr. after a single injection of progesterone. This suggests that HCG acted directly on the ovary but that progesterone acted indirectly by way of the hypothalamo-hypophysial system. Animals injected with progesterone after 6 weeks of constant light failed to ovulate after single or spaced injections of progesterone at 90 days of constant light while HCG administration was still effective. Pituitary content and concentration of luteinizing hormone (LH) in constant-light animals (duration of constant light: 45 days) were below normal pituitary levels during prooestrus and were in the range of normal oestrous values. On the other hand, follicle-stimulating hormone (FSH) content and concentration were similar to those in cyclic rats. Single injections of 1 mg. progesterone changed neither LH nor FSH concentration, despite the fact that such treatment induced ovulation. Bilateral ovariectomy increased both LH and FSH content and concentration in constant-light animals to the same extent as in control light—dark animals.
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SUMMARY
Ovulation-inducing effects of pregnant mare serum gonadotrophin (PMSG) were studied in immature female rats treated on day 5 (day 1 = day of birth) with oil or with 5 or 1250 μg testosterone propionate (TP). The response of rats treated with 1250 μg TP was negligible regardless of the age of the animals and of the dose of PMSG. The response of rats treated with 5 μg TP to PMSG alone was low (36% of rats, with 2·6 ova/ovulating rat), but could be improved by progesterone administration 2 days after PMSG injection (91% of rats, with 14·5 ova/ovulating rat). At every age and dose of PMSG tested the response of animals treated with 5 μg TP to combined PMSG and progesterone treatment was less than that of control animals.
It is concluded that neonatal TP treatment diminishes the release of endogenous ovulating hormone subsequent to PMSG injection. This effect is dependent on the dose of TP used, but already demonstrable in animals treated with 5 μg TP on day 5, which would have been cyclic and fertile after puberty.
Only for the animals treated with 1250 μg TP could a decreased sensitivity of the ovaries to combined administration of PMSG and human chorionic gonadotrophin be demonstrated.
