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PubMed1984

Evidence against a role of prolactin in the timing of ovulation in the turkey.

Two separate experiments in which blood was sampled at 2-h intervals from turkeys hens failed to show a significant change in plasma prolactin (Prl) concentrations in relation to the preovulatory surge of luteinizing hormone (LH) for the first (C1) ovulation of a sequence. Intravenous injection of 125 IU of ovine Prl (NIH-P-S10) or of 1 or 2 ml of antiserum to turkey Prl at varying intervals before C1 ovulation had no effect on the timing or incidence of C1 ovulation. However, injection of Prl before C1 ovulation tended to inhibit ovulation of the second (C2) egg of the sequence, while injection of antiserum to Prl before C1 ovulation tended to either advance or inhibit C2 ovulation. Possibly, the effects of Prl and Prl antiserum on C2 ovulation reflect interference with maturation of the C2 ovarian follicle rather than interference with neuroendocrine processes that regulate the timing of the preovulatory surge of LH. The data for C1 ovulation argue against a change in circulating levels of Prl as a factor in the timing of the preovulatory surge of LH.

Animals↗
PubMed1984

Dissociation of copulation from ovulation in pregnant rabbits.

Experiments were designed to determine why copulation in the pregnant rabbit does not terminate pregnancy while treatment with ovulatory doses of luteinizing hormone (LH) human chorionic gonadotropin (hCG) or luteinizing hormone-releasing hormone (LHRH) is known to do so. Pregnant rabbits (Day 8) were mated or were injected with hCG (25 IU/doe) or LHRH (1, 10 micrograms/kg). Serial blood samples were collected over the next 72 h and analyzed for content of LH, follicle-stimulating hormone (FSH) and progesterone. At sacrifice, uteri and ovaries from these animals were examined for viability of the embryos and for signs of recent ovulation. Injection of hCG or LHRH into pregnant animals led to ovulation and to patterns of LH, FSH and progesterone secretion like those which precede ovulation in estrous rabbits. However, mating the pregnant does did not lead to ovulation or to any changes in the circulating hormones. To investigate whether the elevated levels of progesterone during pregnancy were responsible for the dissociation of coitus from ovulation, nonpregnant rabbits were injected with progesterone (2 mg/kg) and then mated or injected with hCG or LHRH. In virtually every respect, the numbers of ovulations and the patterns of hormone secretion in the progesterone-treated, nonpregnant rabbits mimicked those observed in the 8-day pregnant animals; injection of hCG or LHRH caused ovulation and hormonal surges while hCG caused ovulation only. Mating did not lead to ovulation or any change in blood levels of LH, FSH or progesterone. Taken together, the results show that the elevated circulating levels of progesterone, characteristic of pregnancy, are probably responsible for the dissociation of copulation from gonadotropin release in pregnant rabbits.

Animals↗
PubMed1987

Cyclic adenosine 3',5'-monophosphate-induced ovulation in the perfused rat ovary and its mediation by prostaglandins.

The role and mechanism of action of cyclic adenosine 3',5'-monophosphate (cAMP) in the ovulatory process was investigated by using the in vitro-perfused rat ovary model. Ovaries of pregnant mare's serum gonadotropin (PMSG, 20 IU)-primed rats were perfused for 21 h beginning in the morning of induced proestrus. In vitro stimulation with luteinizing hormone (LH; 0.1 micrograms/ml) resulted in 2.4 +/- 0.7 ovulations per treated ovary. Ovulations could also be induced by the addition of forskolin (30 microM) or dibutyryl cAMP (dbcAMP, 1 mM) with isobutylmethylxanthine (IBMX, 0.2 mM), with 11.8 +/- 1.9 and 18.6 +/- 4.4 ovulations per treated ovary, respectively. Indomethacin (5 micrograms/ml) significantly decreased the number of ovulations in the forskolin and dbcAMP + IBMX groups. The addition of prostaglandin E2 (PGE2; 1 micrograms/ml three times during the perfusion) to the forskolin + indomethacin group reversed the inhibition of ovulation (21.6 +/- 5.4 ovulations per treated ovary). Ovarian PGE tissue levels were significantly higher 10 h after stimulation with either LH, forskolin, or dbcAMP + IBMX compared to the unstimulated control group. Ovulated oocytes in the LH and forskolin groups resumed meiosis but oocytes in the dbcAMP + IBMX groups remained immature. This study shows that an increase in ovarian cAMP, even if not induced by LH, is sufficient to cause ovulation of preovulatory rat follicles, supporting the involvement of cAMP in the normal ovulatory process of the PMSG-treated rat. Furthermore, prostaglandin involvement in cAMP-induced ovulations is demonstrated.

Animals↗
PubMed1993

Involvement of protein kinase C in agonist-stimulated goldfish ovulation.

The effects of two protein kinase C (PKC) inhibitors, calphostin C and staurosporine, on the in vitro ovulation of goldfish (Carassius auratus) oocytes were investigated. Ovulation was stimulated by prostaglandin (PG) F2 alpha (PGF2 alpha, 2.0 micrograms/ml), by sodium orthovanadate (0.1 mM), by a combination of the phorbol ester phorbol 12-myristate-13-acetate (PMA, 0.1 micrograms/ml) and calcium ionophore A23187 (0.05 micrograms/ml), by thapsigargin (0.2 micrograms/ml), and by elevated pH (8.1). In addition, the effects of these inhibitors on the PKC activity of the goldfish follicle wall was determined by use of a specific peptide substrate phosphorylation assay. At 0.1 microM, staurosporine significantly blocked ovulation induced by all agents. However, at lower (0.01 microM) levels it blocked only PMA/A23187-induced ovulation. In contrast, calphostin significantly blocked only PMA/A23187-induced ovulation, although there was a decrease in pH-induced ovulation at lower calphostin concentrations. Both calphostin and staurosporine blocked follicular PKC activity at levels that were inhibitory to ovulation. In addition, staurosporine significantly blocked PKC activity at levels even lower than those needed to block ovulation. The combined results suggest that orthovanadate, PGF2 alpha, and thapsigargin do not require PKC activation for the induction of ovulation, whereas PMA/A23187 does.

Alkaloids↗
PubMed1998

Effects of interleukin (IL)-6 on luteinizing hormone- and IL-1beta-induced ovulation and steroidogenesis in the rat ovary.

Evidence that cytokines have important roles in ovulation is accumulating, with various cytokines having been found to influence the ovulatory cascade. Interleukin (IL)-6 is a pluripotent cytokine involved in inflammatory reactions, and it has been demonstrated in high concentrations in human ovarian follicular fluid and in vitro in secretions from the ovary. We set out to determine the effect this cytokine has on ovulation rate and steroidogenesis in the in vitro-perfused rat ovary. Preovulatory ovaries were taken from eCG-primed animals, and ovulation was induced by LH (100 ng/ml) alone or in combination with cytokine. Ovaries in the IL-6/LH groups (IL-6 concentration of 0.19 nM or 1.9 nM) did not have ovulation rates different from ovaries in the LH-only group. Ovaries in the LH/IL-1beta group ovulated more oocytes than ovaries in the LH-only group (LH/IL-1beta =11+/-1.8 oocytes; LH alone=4.9+/-1.1; p=0.015) and the IL-6/LH/IL-1beta group (LH/IL-1beta/IL-6 [0.19 nM]=4+/-1.40; LH/IL-1beta=11+/-1.8; p=0.009). We have found that 1) exogenous IL-6 did not significantly alter the LH-induced ovulation rate but significantly reduced the LH/IL-1beta-induced ovulation rate; 2) exogenous IL-6 did not alter LH-induced progesterone levels measured at time points during the perfusion period, but the average increase in progesterone over basal level was stimulated by IL-6; 3) exogenous IL-6 did not affect LH-induced estradiol production; 4) exogenous IL-6 did not affect LH-induced androstenedione production but increased LH/IL-1beta-induced production; 5) exogenous IL-6 did not affect LH-induced prostaglandin E2 production. This study demonstrates that IL-6 does not play a role in regulating ovulation induced by LH in vitro but is capable of reducing LH/IL-1beta-enhanced ovulation rates. In addition, IL-6 may play a role in the regulation of ovarian steroid production.

Animals↗
PubMed2001

Evidence that an imprinted gene on the X chromosome increases ovulation rate in sheep.

Ovulation rate records from 1311 female progeny of 50 Coopworth rams were used to study the inheritance of ovulation rate in a screened high prolificacy sheep flock. Breeding values (BV) for ovulation rate for 33 sires used within the screened flock and ovulation rate deviations for a further 17 sires progeny tested in commercial flocks suggest that a major gene (WOODLANDS: gene) for ovulation rate with a non-Mendelian inheritance pattern is segregating in a family line. Rams assigned as carriers of the putative gene did not produce carrier sons (zero of three), and this coupled with the observation that daughters of carrier rams had ovulation rates of 0. 39 (standard error of difference [SED] = 0.06) higher than contemporaries without a significant increase in the variance of log ovulation rate strongly suggests that the gene is on the X chromosome. The evidence suggests that the gene is also maternally imprinted because ovulation rate data indicate that it is expressed where females inherit a paternal allele but is silenced when inherited on a maternal allele. Maternal granddaughters of carrier rams had mean ovulation rates that were only 0.02 (SED = 0.06) higher than noncarrier ewes from the same flock. Furthermore, carrier dams expressing the gene (paternal allele) had 24 sons, none of which had female offspring that expressed the gene, whereas carrier dams not expressing the gene (maternal allele) had 7 out of 17 sons that had female progeny expressing the gene. There is no evidence of the infertility that occurs in homozygous ewes carrying the X-linked Inverdale gene. Collectively, these results suggest the existence of a novel gene for prolificacy located on the X chromosome that is maternally imprinted. The WOODLANDS: gene was only expressed upon paternal inheritance from carrier males that were the progeny of nonexpressing carrier dams. The gene was not expressed in ewes that received it from either carrier dams (expressing or nonexpressing) or from carrier males that were the progeny of expressing carrier dams.

Animals↗
PubMed1997

Reproductive efficiency in the common marmoset (Callithrix jacchus): a longitudinal study from ovulation to birth monitored by ultrasonography.

This study examines reproductive efficiency in the common marmoset monkey, Callithrix jacchus, using sequential ultrasound examinations to establish ovulation number, implantation rate, and incidence of prenatal loss. Ultrasound was carried out with a 10 or 7.5 mHz probe in nonsedated animals, daily during the late follicular phase, approximately twice a week until day 20 after ovulation, and at days 35, 56, and 85 of pregnancy to enable visualization of gestation sacs, heartbeats, and fetal heads, respectively. Ovulatory follicles could be seen 3-4 days before ovulation and by day -2, 98% of ovulating follicles were > 2mm diameter, although almost 10% of follicles of this size disappeared without ovulating. Total number of ovulating follicles for 15 females was 45 (mean ovulation rate = 3.0, range 2-4). In the 14 animals that conceived, 41 corpora lutea were identified (mean ovulation rate = 2.9) within 10 days of ovulation. All pregnancies went to term (no abortion occurred) resulting in the birth of 37 neonates (9 triplets, 5 twins) and an average litter size of 2.64. All four losses were confined to the embryonic period (< day 85), two occurring before day 35, one between days 35 and 56, and one between days 56 and 85. In demonstrating that 90% of ovulatory follicles gave rise to live offspring, the results of this study indicate an extremely high reproductive efficiency in the marmoset monkey (when maintained under favorable captive conditions) and a rate of prenatal loss much lower than that reported for other primate species.

Animals↗
PubMed2002

The effect of timing of administration of oestradiol benzoate on characteristics of oestrus, timing of ovulation and fertility in Bos indicus heifers synchronised with a progesterone releasing intravaginal insert.

OBJECTIVE: To compare the timing of onset of oestrus and ovulation, characteristics of oestrus, and fertility in Bos indicus heifers synchronised with a progesterone releasing intravaginal insert (IVP4) and administration of oestradiol benzoate (ODB) either at the time of removal of the insert or 24 h later. DESIGN: Cohort study. PROCEDURE: Bos indicus and Bos indicus cross heifers were treated on two farms (Farm A, n = 273; Farm B, n = 47) with an IVP4 for 8 days with 1.0 mg of ODB administered at the time of device insertion and 250 mg of cloprostenol at the time of device removal. Heifers in the ODB-0 group were administered 0.75 mg of ODB at the time of device removal while heifers in the ODB-24 group were administered the same dose of ODB 24 h after device removal. Heifers were inseminated once daily after detection of oestrus. Heifers not detected in oestrus by 72 h after removal of inserts were inseminated at that time. Oestrus was detected in heifers on Farm A using heatmount detectors while on Farm B oestrus in heifers was monitored using radiotelemetry of mounting pressure. Ovarian follicular development was monitored daily in 30 heifers on Farm B from the time of administration of inserts until ovulation to a maximum of 96 h after removal of inserts, and again 11 days after removal of inserts (Day 19). A blood sample was collected from all heifers on Farm B on Day 19 and analysed for plasma concentration of progesterone. Pregnancy was diagnosed 6 to 8 weeks after insemination. RESULTS: Administration of ODB at the time of removal of inserts shortened the time interval to oestrus and ovulation (P < 0.001), increased the number of mounts recorded during oestrus (P = 0.04) and reduced the odds of pregnancy (P = 0.03). The proportion of heifers ovulating on Farm B was 67% and was not affected by treatment group (P = 0.61). The mean diameter of the largest follicle measured in ovaries was greater at the time of removal of inserts (9.1 +/- 0.6 vs 10.7 +/- 0.4; P = 0.03) and at the expected time of the LH surge (8.1 +/- 0.4 vs 11.5 +/- 0.3 mm; P < 0.001) in heifers that ovulated compared to heifers that failed to ovulate, respectively. Emergence of a new follicular wave was not detected during the synchronisation treatment in heifers that failed to ovulate. Concentrations of progesterone in plasma on Day 19 were less in non-pregnant heifers (P = 0.05) compared to heifers subsequently diagnosed as pregnant to insemination and were affected by the diameter of the ovulatory follicle (P = 0.01). CONCLUSION: Administration of ODB at the time of removal of inserts can shorten the time interval to oestrus and ovulation and can reduce fertility when insemination is carried out once daily. Further work is needed to determine if prolonged suppression of follicular development, anovulatory oestrus and premature ovulation occuring in some heifers is associated with administration of ODB.

Administration, Intravaginal↗
PubMed1989

Neuroendocrine effect of toki-shakuyaku-san on ovulation in rats.

In this study, the experiments were designed to examine if Toki-Shakuyaku-San (TSS) has a neuroendocrine effect on ovulation. TSS (500 mg/kg Bwt in drinking water) was given to Sprague Dawley immature female rats on 25 days of age and during experimental sessions. Fifteen IU of the hMG (Gonadoryl 4; GNR 4) was injected intraperitoneally on the morning of 28 days of age, and ovulation occurred in 70% of rats on the following day. In TSS drinking immature female rats, administration of GNR 4 on 28 days of age results in ovulation twice: once on 29 days of age and again on 31 days of age. Administration of sodium pentobarbital (Nembutal) at 12:30 p.m. on 28 days of age did not block the first ovulation on 29 days of age, but administration at 12:30 p.m. on 30 days of age blocked the second ovulation on 31 days of age. However, delayed ovulation was observed on 32 days of age. This evidence indicates that GNR 4 acts on the ovary directly and induces first ovulation in TSS treated rats. However, TSS treatment modulates the chain of events in the neuroendocrine control of ovulation and results in the second ovulation.

Animals↗
PubMed1977

Blockade of LH release and ovulation in the rabbit with inhibitory analogues of luteinizing hormone releasing hormone.

Plasma LH levels and ovulation were studied in female rabbits following administration of several inhibitory analogues of luteinizing hormone-releasing hormone (LHRH) before and after mating with experienced males. Administration of (D-Phe2, D-Leu6)-LHRH (1.5 mg/kg sc) to does 30 min before mating did not prevent either LH release or ovulation. However, a single sc injection of (D-Phe2, L-Phe3, D-Phe6y-LHRH (6 mg/kg) given 30 min before mating in 4 rabbits resulted in a 30-60 min delay in the coitus-induced release of LH when compared with post-coital changes in the same animals injected with vehicle; however, all of the does ovulated. When multiple dosages of 4 mg/kg (D-Phe2, L-Phe3, D-Phe6)-LHRH were administered 3-5 times at half-hourly intervals beginning 30 min prior to mating there was a considerable reduction in plasma LH elevations at 0.5, 1.0, 2.0 and 4.0 h after mating and 3/5 treated rabbits showed partial or complete blockade of ovulation. Quite similar results were obtained with the same dosage of (D-Phe2, D-Trp3, D-Phe6)-LHRH. An early sharp peak in LH release and full ovulation were stimulated in 6 out of 6 does by a single iv injection of synthetic LHRH (500 ng/kg). However, in another experiment, three half-hourly sc injections (4 mg/kg) of (D-Phe2, L-Phe3, D-Phe6)-LHRH beginning 30 min before administering LHRH markedly reduced the rise in plasma LH (P less than 0.01) and completely blocked ovulation in all of the same 6 animals. An unsuccessful attempt was made to provide a test animal for LHRH analogue investigations by implanting 4 cm of silastic tubing filled with crystalline estradiol (E2) sc in ovariectomized (OVX) AND INTACT DOES. In OVX does the silastic E2 implants resulted in a progressive decline in the ability to release LH in response to mating at 6 and at 20 days after implantation. With ovaries present, the E2 implant permitted post-coital LH release and ovulation at 4 d but not at 30 d post-implantation. At 30 d after removal of the E2 implant three out of four does had fully recovered the ability to release LH and ovulate post-coitally. Collectively, these results indicate that inhibitory analogues of LHRH can effectively block the ovulatory response to exogenous LHRH in rabbits, but that coitally-induced LH release and ovulation are less susceptible to blockade by the analogues. Silastic E2 implants, however, progressively and reversibly reduce the capacity of does to release LH after mating.

Animals↗
PubMed1980

Effect of copulatory stimuli on incidence of ovulation and on serum luteinizing hormone in the cat.

The relationship among the number of copulatory stimuli, the incidence of ovulation, and the pituitary release of LH was studied in the female cat (queen), an induced or reflex-ovulating species. Estrual queens were mated with a male either once during estrus (on day 1, 2, 3, or 4) or three times at 4-h intervals in a single day of estrus (on day 1, 2, or 3). Laparoscopy was used to examine the ovaries, initially to determine the numbers of preovulatory follicles and later to count corpora lutea. Blood samples were obtained serially from cats in each mating group, and sera were analyzed for LH. The day of estrus on which mating occurred, estrus duration, and follicle numbers had no effect on the proportion of animals ovulating. A single mating resulted in fewer queens ovulating per group (10 of 48 animals) than three matings on a single day (30 of 36). After copulation, LH was elevated only in animals later confirmed to ovulate. LH response in ovulating queens varied among individuals but, when averaged, appeared to be greater and more prolonged in multiple mated vs. single mated animals. These data indicate that the reflex-ovulating cate does not always ovulate after a single copulatory stimulus because of a failure of LH release. The frequency of coital stimulation apparently plays a major role in influencing the proportion of animals ovulating, with multiple copulation apparently enhancing the pituitary release of LH.

Animals↗
PubMed1986

Effect of time and dose of indomethacin on follicular prostaglandins and ovulation in the rabbit.

This study determined specifically when ovarian prostaglandins (PGs) increase during ovulation and how effectively different doses of indomethacin inhibit PGs and ovulation. Rabbit ovarian follicles were removed at hourly intervals after stimulating the animals with hCG (50 IU/kg). The follicles were homogenized in 0.1 M acetate buffer (pH 4.5), and the PGE and PGF in the extracts were measured by RIA. Ovulation rates were determined by calculating the percentage of mature follicles that ruptured after stimulation by hCG. Before hCG, the normal levels of PGE and PGF were 111.1 +/- 14.7 and 51.0 +/- 6.6 pg/mg follicle, respectively. By 2 h after hCG treatment, PGE and PGF both increased to 162.6 +/- 17.0 and 80.6 +/- 13.3 pg/mg follicle, respectively. Approximately 5 h later, there was a second, sharper increase in both PGs which peaked at 652.6 +/- 63.5 and 345.4 +/- 32.3 pg/mg follicle, respectively, 10 h after hCG treatment, i.e. at the expected time of ovulation. We found that regardless of whether indomethacin was given early or late during the ovulation process, this agent significantly reduced follicular PG production within 5 min after its administration. For example, only 5 min after 10 mg/kg indomethacin were administered 8 h after hCG, PGE and PGF dropped from 317.7 +/- 50.0 and 125.0 +/- 10.5 pg/mg follicle to 93.3 +/- 17.4 and 49.3 +/- 10.5 pg/mg follicle, respectively. Unexpectedly, when graded doses of indomethacin were administered either 1 or 8 h after hCG, there was not a statistically significant correlation between follicular PG levels and ovulation rate. For example, when doses of 1.25, 2.5, 5.0, and 10.0 mg/kg indomethacin were given 8 h after hCG, the PGE and PGF levels at the expected time of ovulation (i.e. 2 h later) were always equal to or less than the PG levels in follicles that had not been stimulated by hCG, yet ovulation proceeded at rates of 46.7 +/- 12.3%, 30 +/- 7.7%, 14.3 +/- 9.3%, and 0%, respectively. Therefore, the results raise questions about the specific role of PGs in the ovulation process.

Animals↗
PubMed1989

Suppression of ovulation rate by antibodies to tissue-type plasminogen activator and alpha 2-antiplasmin.

Indirect evidence has suggested a role for plasminogen activator (PA) in ovulation. Our recent studies demonstrated that 1) tissue-type PA (tPA) is the predominant PA produced by preovulatory rat follicles in response to gonadotropins or GnRH; and 2) several inhibitors of the serine proteases, to which PA and plasmin belong, block ovulation. Here, the role of tPA and plasmin in ovulation was examined directly by the use of specific antibodies to tPA and alpha 2-antiplasmin (alpha 2AP). Immature female rats at 25-26 days of age were treated (sc) with 15 IU PMSG to induce multiple preovulatory follicles. Fifty-four hours later, tPA antibodies and alpha 2AP were injected into one of the ovarian bursae to check their ability to block ovulation, which was initiated with an ovulatory dose (4 IU) of hCG. The data are expressed as percent inhibition of ovulation in the treated vs. the untreated ovaries. A significant decrease in the ovulation rate was obtained by administration of 500 micrograms antibodies to tPA (39.6%) or 1-50 micrograms alpha 2AP (36-44%), whereas minimal inhibition (12%) was found at lower doses of anti-tPA (10 micrograms) or alpha 2AP (0.1 micrograms). Furthermore, nonimmune immunoglobulin G (500 micrograms) and heat-inactivated alpha 2AP were not effective. Anti-tPA and alpha 2AP suppressed ovulation only when injected at the time of hCG administration; later injections (4-h delay) were ineffective, suggesting that PA and plasmin are involved in the early follicular responses to the ovulatory stimulus. Histological observation of the ovaries did not reveal any pathological changes associated with the anti-tPA and alpha 2AP treatment. Suppression of ovulation, as evidenced by decreased number of tubal ova, was frequently accompanied with intraovarian release of the eggs into the follicular thecal compartment. Thus, these results provide direct evidence for an essential role of tPA and plasmin in ovulation.

Animals↗
PubMed1975

Precocious puberty: the effect of adrenalectomy on PMS-induced ovulation and progesterone secretion.

Female Sprague-Dawley derived rats were received at 21 days of age and either sham-operated or adrenalectomized on that day. Half of the animals received either 25 IU pregnant mare's serum gonadotrophin (PMS) or 0.9 saline at 9 AM on the next day; the other half were injected at 26 days of age. On the day of expected ovulation (days 24-25 and days 28-29) the rats were killed at 4-hr intervals and the incidence of ovulation determined. Serum progesterone and corticosterone were measured with the intent of comparing the pattern of these steroids with the timing and incidence of ovulation. Twenty-two-day-old rats given PMS ovulated later (at 0400 on day 25) than did the 26-day-old rats (at 2400 on day 28). Adrenalectomized ADRX rats ovulated later than intact controls at both ages (ovulation complete at 1600 on days 25 and 29, respectively). There was a reduced ovarian weight response to PMS in ADRX rats but uterine weights were not consistently different from intact PMS-treated rats. Associated with the different timing of ovulation and organ weight response in the ADRX rats there was a lower serum progesterone response on days 24-25. In intact PMS-treated rats, the rhythm of the serum corticosterone was different in the two age groups. It is concluded that adrenalectomy alters the normal response to PMS resulting in a delay in the time of ovulation. It is possible that the adrenal normally participates in the induction of ovulation after PMS, possibly by acting as an internal priming agent to facilitate gonadotrophin release in the young rat.

Adrenal Glands↗
PubMed1976

Luteinizing hormone requirements for ovulation in the pentobarbital-treated proestrous rat.

The LH requirements for ovulation in the pentobarbital-blocked proestrous CD rat have been studied by increasing serum gonadotropin levels through electrical stimulation of the brain and subsequently comparing the effects of timed hypophysectomy on ovulation and serum LH concentrations. The arcuate nucleus (ARC) or the medial preoptic area (POA) was stimulated unilaterally for 45 min with matched pairs of biphasic rectangular pulses through a coaxial platinum electrode. Serum LH was significantly elevated above basal values at the end of stimulation, but not in sham-stimulated controls. The results of both hormone measurement and hypophysectomy showed that the pituitary continued to release LH after extrinsic stimulation of the hypothalamus had ceased. Animals did not ovulate if they had been hypophysectomized at the end of the 45 min stimulation whereas nearly all ovulated if hypophysectomy was delayed for an additional 20 min. Some evidence suggested that the pituitary could be removed earlier without affecting ovulation if the rate of LH release was increased. The minimum peak LH concentration measured in rats that subsequently ovulated fully was 187 ng/ml, substantially lower than concentrations ordinarily attained in the spontaneous proestrous surge. When serum LH was insufficiently high to cause follicle rupture, there was nevertheless the resumption of meiosis and luteinization of the large ovarian follicles. Attempts were made to restore ovulability in animals presumed to have released a subovulatory quota of gonadotropin. Ovulation was obtained when such animals, prepared by hypophysectomy after the 45 min stimulation, had been bilaterally nephrectomized prior to stimulation. However, multiple injections of progesterone after hypophysectomy were without effect. The results are discussed in relation to variables that affect minimum requirements of LH for ovulation.

Animals↗
PubMed1993

Interleukin-1 beta (IL-1 beta) modulates prostaglandin production and the natural IL-1 receptor antagonist inhibits ovulation in the optimally stimulated rat ovarian perfusion model.

The rat ovarian perfusion model with bursa removed and intact was used to further characterize the effects of interleukin-1 beta (IL-1 beta) and the natural IL-1 receptor anatagonist (IRAP) on ovulation, steroidogenesis, and prostaglandin production. Twenty-six- to 27-day-old female Sprague-Dawley rats were injected sc with 25 IU PMSG, and 48 h later, the right ovary was dissected (with bursa removed and intact for various experiments) and placed in the perfusion chamber. Ovaries were exposed to various doses of IL-1 beta alone, IL-1 beta with LH, and IL-1 beta with LH and isobutylmethylxanthine (IBMX). The natural IL-1 receptor antagonist was also added to the chambers with LH and IBMX. IL-1 beta at 0.8 (n = 3) and 8.0 (n = 4) nM did not induce LH-independent ovulation in PMSG-stimulated ovaries with bursa removed. In bursa-intact perfusions (n = 3), one ovulation was produced in each compared to control ovaries with bursa intact (n = 3) given an ovulatory trigger of LH alone [2.3 +/- 0.6 (+/- SD) ovulations; P < 0.02]. IL-1 beta enhanced, in a dose- and gonadotropin-dependent fashion, the production of prostaglandin E2 (PGE2) in PMSG-stimulated ovaries with bursa removed given an ovulatory trigger of LH and IBMX compared to that in controls. PGF2 alpha and 6-keto-PGF1 alpha were also modulated by IL-1 beta. Estradiol and progesterone production were not affected. The natural IRAP inhibited ovulation (7.8 +/- 3.9 ovulations vs. 12.4 +/- 1.5; P < 0.04) in PMSG-stimulated ovaries given LH and IBMX as the ovulatory trigger compared to that in controls. This inhibition of ovulation was not associated with reduced steroid or PG levels. IL-1 beta appears to play a potentially significant role in the process of ovulation. The functional importance of the bursa in this model is highlighted in this study. IL-1 beta modulates PG, but not steroid, production. IRAP inhibited ovulation without significantly affecting PG or steroid production.

1-Methyl-3-isobutylxanthine↗
PubMed1998

The role of nitric oxide in oocyte meiotic maturation and ovulation: meiotic abnormalities of endothelial nitric oxide synthase knock-out mouse oocytes.

Evidence supports the involvement of nitric oxide (NO) in ovulation, steroidogenesis, and atresia-related apoptosis. This study was designed to investigate the role of endothelial nitric oxide synthase (eNOS)-derived NO in ovulation, oocyte meiotic maturation, and ovarian steroidogenesis using wild-type (WT) mice and mice in which the gene for eNOS had been deleted (eNOS knock-out). We observed that mature eNOS knock-out females have significantly fewer pups born in each litter and a higher mortality rate of pups than those born to heterozygote or WT females (P < 0.05). To determine the influence of eNOS deficiency on ovarian function, immature WT and eNOS knock-out mice were superovulated by injecting PMSG (5 IU) followed by an injection of hCG (5 IU, i.p.) 48 h later. To determine whether murine oocytes expressed eNOS before (0 and 8 h post-hCG) and after ovulation (16 h post-hCG). we performed immunofluorescent staining. Positive specific staining for eNOS was observed on the surface of ovarian and ovulated oocytes obtained from WT mice, but not on oocytes from eNOS knock-out mice. To determine the role of eNOS-derived NO in ovulation, ovulated oocytes were counted 16 h post-hCG. eNOS knock-out females showed a significant reduction (by 63%; P < 0.0001) in ovulatory efficiency compared with WT females. The reduction in the ovulation rate in eNOS-deficient mice compared with that in WT mice was also associated with a higher concentration of estradiol (P < 0.01) without significant changes in the plasma progesterone level. eNOS deficiency impaired not only ovulation, but also oocyte meiotic maturation. Ovulated oocytes were classified as being in one of the following stages of meiosis: metaphase I, metaphase II, or showing atypical (degenerative) morphology. We observed that fewer oocytes from eNOS knock-out mice had entered metaphase II of meiosis, and a greater percentage remained in metaphase I or were atypical (P < 0.002) relative to those in WT mice. Furthermore, many oocytes that showed either a delay in meiotic maturation or abnormal morphology were undergoing cell death. Our results support a role for NO in the ovulatory process. The ovarian defects observed in the eNOS knock-out mice suggest that eNOS-derived NO is a modulator of oocyte meiotic maturation.

Animals↗
PubMed1989

Blood LH level and induced ovulation after hCG and PMSG treatment in ovarian quiescent cattle.

Ovarian quiescent cattle bearing follicle with palpable size were treated with single intramuscular injection of 750-6,000 IU of human chorionic gonadotrophin (hCG) in 13 cases and 1,000-2,000 IU of pregnant mare serum gonadotrophin (PMSG) in 5 cases. Changes of blood luteinizing hormone (LH) level, estrus and ovulation after the treatments were examined. After the hCG treatment LH level became slightly high from 0.2-0.6 ng/ml of pre-treatment to 0.3-1.9 ng/ml of post-treatment and maintained the level up to ovulation without the ovulatory LH surge. Ovulation was induced about 36 hr after the treatment in 12 cases. The ovulations were all silent ovulations. After the PMSG treatment LH level became slightly high from 0.6 ng/ml of pre-treatment to 1.3 ng/ml of post-treatment and the level lasted until the ovulatory LH surge. The ovulatory LH surge occurred about 39 hr after the PMSG treatment in 4 cases with a peak of about 32 ng/ml. Ovulation was induced about 74 hr after the treatment in all 5 cases. Four cases showed estrus but one in which the LH surge could not be confirmed did silent estrus preceding the induced ovulations. It was demonstrated that hCG induced ovulation without the LH surge but PMSG induced the ovulatory LH surge and the subsequent ovulation in ovarian quiescent cattle.

Animals↗