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Metallo-protease activity increases prior to ovulation in brook trout (Salvelinus fontinalis) and yellow perch (Perca flavescens) follicle walls.

Proteolytic activity was measured in the follicle wall surrounding oocytes from brook trout (Salvelinus fontinalis) and yellow perch (Perca flavescens) by use of two different protease assays: sodium dodecyl sulfate-polyacrylamide gel electrophoresis (substrate-SDS-PAGE) and a chromogenic synthetic peptide for type I collagen. In brook trout follicle walls, substrate-SDS-PAGE studies demonstrated that the activity of two proteolytic enzymes (80 kDa and 66 kDa) increased significantly before ovulation. The 80 kDa enzyme decreased significantly after ovulation whereas the 66 kDa enzyme remained elevated following ovulation. In yellow perch follicle walls, substrate-SDS-PAGE studies demonstrated that the activity of the major protease (66 kDa) increased before ovulation and remained elevated after ovulation. A chromogenic synthetic peptide was used to assay collagenolytic activity in follicle walls of brook trout and yellow perch. This assay revealed that collagenolytic activity increased significantly in both species before ovulation and remained elevated after ovulation. These findings suggest that metallo-proteases are involved in digesting the follicle wall in teleosts before and after ovulation.

Animals↗

Orthovanadate and fluoroaluminate stimulate inositol phosphate production and in vitro ovulation in goldfish (Carassius auratus) follicles.

Both sodium orthovanadate and fluoroaluminate were found to stimulate in vitro ovulation in intact goldfish follicles, suggesting the involvement of G-proteins in ovulation. Although orthovanadate was able to stimulate cAMP production, it probably stimulates ovulation by some other mechanism since cAMP blocks ovulation in this species. These agents also stimulated the accumulation of labeled inositol phosphate in follicle walls. The time course of inositol phosphate production showed a slightly delayed and continuous accumulation for isomers of inositol mono-, bis-, and trisphosphates. No change was observed in inositol tetrakisphosphate levels over time. The accumulation of inositol phosphates in response to orthovanadate was also dose-dependent. Lithium chloride (10 mM) caused varying increases in the levels of most isomers and a decrease in ins-3,4-P2. Inositol phosphate production varied significantly with changes in the maturational stage of follicles. Peak production was observed in follicles 7-8 h after hCG treatment, which corresponds almost exactly with the time of ovulation. This correlation of maximal inositol phosphate production with the time of ovulation, along with the stimulation of ovulation by diacylglycerols, a phorbol ester, and the G-protein-stimulating agents, orthovanadate and fluoroaluminate, suggests a role for polyphosphatidylinositol hydrolysis in ovulation.

Aluminum↗

Inhibition of ovulation in the perfused rat ovary by the synthetic collagenase inhibitor SC 44463.

A new, powerful, synthetic inhibitor of mammalian tissue collagenases and related metalloproteinases is inhibitory to ovulation in perfused rat ovaries. Ovaries of immature rats, primed with 20 IU of eCG, were dissected and perfused with 0.1 micrograms/ml LH and 0.2 mM 3-isobutyl-1-methylxanthine (IBMX) for 20 h. Addition of SC 44463 (N4-hydroxy-N1-[1S [(4-methoxphenyl)methyl]-2-(methylamino)-2-oxoethyl]- 2R-(2-methylpropyl)butane-diamide) at a concentration of 25 nM inhibited ovulation by 55% (9.6 +/- 1.7 ovulations per ovary, mean +/- SEM, compared to a control value of 21.7 +/- 1.7); and 250 nM inhibited ovulation by 75% (5.3 +/- 1.1 ovulations per ovary). We previously showed that the related compound SC 40827 inhibited ovulation by 70% when used at a concentration of 25 microM (Brännström et al., Endocrinology 1988; 122:1715-1721). We now show that SC 44463 is 100, 500, and 75 times more powerful than SC 40827 in blocking ovulation, inhibiting action of ovarian interstitial collagenase, and inhibiting action of the small metalloproteinase of the rat uterus, respectively. SC 44463 also inhibits ovarian type IV collagen-digesting activity 50% at a concentration of 18 nM. Ovulation occurs after 9-12 h of perfusion with LH. Compound SC 44463 (25 nM) showed its full inhibitory capacity when added to the medium as late as 7 h after LH, but there was no significant inhibition when it was added at 9 h. This suggests that the major collagenolytic events occur beyond 7 h after stimulation by LH.

1-Methyl-3-isobutylxanthine↗

Intrabursal injection of clodronate liposomes causes macrophage depletion and inhibits ovulation in the mouse ovary.

To investigate the role of the ovarian macrophage population in ovulation, we examined the effect of depleting this population using liposome-encapsulated clodronate. Clodronate liposomes, saline liposomes, or saline alone was injected under the ovarian bursa in gonadotropin-primed adult mice, either 84 h (Day -3) or 36 h (Day -1) before ovulation. Ovulation rates were determined by counting the number of oocytes released. The numbers of graafian follicles and corpora lutea were also counted immediately before and after ovulation. Macrophage distribution within the theca and stroma of preovulatory ovaries was examined by immunohistochemistry with specific monoclonal antibodies to the macrophage antigens macrosialin, major histocompatability complex class II (Ia), and F4/80. Injection of clodronate liposomes on Day -1 did not affect ovulation rates, whereas administration on Day -3 caused a significant reduction in ovulation rate (mean oocytes ovulated = 5. 25 +/- 0.6 from clodronate liposome-treated ovaries and 9.13 +/- 0.9 from saline-treated ovaries, respectively, P < 0.05). The numbers of macrosialin-positive macrophages present in the theca at ovulation were reduced by treatment with clodronate liposomes on Day -1, and treatment on Day -3 reduced the numbers of Ia-positive and macrosialin-positive macrophages present in the theca. When the subsequent ovarian cycles were examined by vaginal smearing, the metestrous-2/diestrous stage was found to be extended in clodronate liposome-treated animals (7.5 +/- 1.3 days vs. 3.4 +/- 0.4 days for saline liposome-treated animals, P < 0.05). These results suggest that thecal macrophages may be involved in the regulation of follicular growth and rupture, as well as being important for the normal progression of the estrous cycle.

Analgesics, Non-Narcotic↗

Nutritionally induced anovulation in beef Heifers: ovarian and endocrine function during realimentation and resumption of ovulation.

Nutritionally induced anovulatory and cyclic Angus x Hereford heifers were used to evaluate follicular growth and concentrations of hormones and metabolites during anovulation and resumption of ovulation. Anovulatory heifers were fed to gain 0.6 (LGAIN) or 1.5 (HGAIN) kg/day until resumption of ovulation, and heifers with normal estrous cycles were fed a maintenance diet (M). Follicles >/= 4 mm in diameter were measured by daily ultrasonography in HGAIN and LGAIN heifers during one follicular wave before realimentation (Wan) and in two waves (W-2, W-1) immediately before the wave resulting in first ovulation or luteinization (W0). Ovaries of M heifers were evaluated to determine the day of ovulation of the second-wave dominant follicle (DF). Resumption of ovulation after realimentation occurred 23 days earlier in HGAIN than in LGAIN. Maximum diameter, growth rate, and persistence of dominant follicles increased, while persistence of first subordinate follicles decreased between anovulation and resumption of ovulation in anovulatory heifers. Concentrations of LH in serum were similar for HGAIN and LGAIN and gradually increased during realimentation. The increase in estradiol before the first ovulation was less in realimented heifers compared with cyclic heifers. Concentrations of insulin-like growth factor-I (IGF-I) in HGAIN and LGAIN gradually increased during realimentation but were lower than concentrations of IGF-I in cyclic heifers at ovulation. Increased diameter, growth rate, and persistence of the DF were associated with increased concentrations of LH, estradiol, and IGF-I during the transition from nutritionally induced anovulation to resumption of ovulatory cycles.

Animal Nutritional Physiological Phenomena↗

Time-dependent ovulation inhibition of a selective progesterone-receptor antagonist (Org 31710) and effects on ovulatory mediators in the in vitro perfused rat ovary.

Progesterone (P) is one of several local mediators in the ovulatory cascade in the rat. The precise mechanisms of action for P in ovulation and in what phase of the ovulatory process P is critical, however, need to be clarified. The present study used a selective P-receptor antagonist, Org 31710, in the in vitro perfused rat ovary model to examine the local role of P and possible effects on prostaglandin (PG) and plasminogen-activator (PA) release in ovulation. Ovaries from eCG (15 IU)-primed rats were perfused for 20 h with LH (0.2 microg/ml) and 3-isobutyl-1-methylxanthine (IBMX, 200 microM) to induce ovulation (median = 10.0, 25%-75% range = 8.5-13). Org 31710 was added at either 0, 3.5, 7, or 9 h after LH+IBMX, resulting in significant suppression of ovulation after addition at 0 and 3.5 h (1.0, 1-5.5; and 5.0, 2.5-7.75 ovulations, respectively) but no suppressive effect when added at later time points. Progesterone and estradiol levels in the perfusion media were increased after LH+IBMX but were not affected by the presence of Org 31710. Ovarian tissue levels of PGE(2), PGF(2 alpha), and PA activity were measured in ovaries that had been perfused for 10 h, a time that was 2 to 5 h before anticipated ovulation. The presence of Org 31710 significantly decreased the levels of PGE(2), PGF(2 alpha), and PA activity. These results suggest that P is essential in ovulation during the initial stages of the ovulatory process. The effect of P to facilitate ovulation seems to relate to stimulation of the PG- and PA-mediator systems.

1-Methyl-3-isobutylxanthine↗

Effects of time of insemination relative to ovulation on pregnancy rate and embryonic-loss rate in mares.

The effects of pre-ovulatory and post ovulatory insemination on pregnancy rate and embryonic-loss rate were studied in 268 mares in two experiments. Within each experiment mares were randomised within replicates as follows: to be inseminated on the day the pre-ovulatory follicle reached 35 mm (pre-ovulatory group), to be inseminated on the day of ovulation (Day 0 group), and to be inseminated on the day after ovulation (Day 1 group). Ultrasonic pregnancy diagnoses were performed on Days 11, 12, 13 and 14 (Experiment 1) and Days 11, 12, 13, 14, 15, 20 and 40 (Experiment 2). Combined for the two experiments, pregnancy rates were different (P less than 0.01) among the three groups. For Experiment 2, pregnancy rate within the pre-ovulatory group was lower (P less than 0.05) for insemination 4 days or more before ovulation than for up to 3 days before ovulation. Pregnancy rate was lower (P less than 0.05) for the Day 0 group than for the pre-ovulatory group inseminated up to 3 days before ovulation. In Experiment 2, ovulation was detected by examinations every 6 h; pregnancy rate was greater (P less than 0.05) for mares inseminated 0 to 6 h after ovulation than for mares inseminated at 18 to 24 h. No pregnancies occurred when mares were inseminated 30 h or more after ovulation. The mean day of first detection of the embryonic vesicle was different (P less than 0.0001) among the three groups. Diameter of embryonic vesicle averaged over Days 11 to 15 also differed (P less than 0.0001) among groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of toki-shakuyaku-san on ovulation induced by human menopausal gonadotropin in rats.

One hundred and thirty-five immature female rats were treated with Toki-Shakuyaku-San (TSS:500 mg/kg, Bwt in drinking water) beginning at 25 days of age and continuing during experimental sessions. Fifteen IU of the human menopausal gonadotropin (hMG:Gonadoryl:GNR:GNR 4 contains 4 to 1 ratio of FSH and LH) was injected intraperitoneally on the morning of 28 days of age, and ovulation (presence of tubal ova) was examined on the morning of 29, 30 and 31 days of age. GNR 4 alone induced ovulation at 29 days of age (70%) and at 30 days of age (35%); however, no ovulation was observed at 31 days of age. TSS treatment alone causes 30% to ovulate at 31 days of age. When GNR 4 was combined with TSS treatment, animals demonstrated ovulation at 31 days of age, that is, they ovulated at 29 days of age (93%), at 30 days of age (30%) and at 31 days of age (90%). These results infer that TSS treatment may accelerate the chain of events in the neuroendocrine control on ovulation, thus causing more frequent ovulation in rats.

Animals↗

Oxoanions stimulate in vitro ovulation and signal transduction pathways in goldfish (Carassius auratus) follicles.

The present study investigated the effects of a number of oxoanion compounds on in vitro ovulation of goldfish follicles and ovarian second messenger activities. Significant levels of ovulation were induced by 0.1 mM sodium chromate, 0.1 mM sodium metavanadate, 10 mM sodium molybdate, 0.1 mM sodium orthovanadate, 5 mM sodium selenate, 0.5 mM sodium tungstate, and 0.1 mM vanadyl sulfate. At levels that significantly stimulated ovulation, metavanadate, molybdate, orthovanadate, tungstate, and vanadyl sulfate also stimulated follicular phosphatidylinositol cycling and inhibited ovarian alkaline phosphatase activity. Moreover, the ovulation induced by these oxoanions was not inhibited by indomethacin (10 micrograms/ml), while ovulation induced by selenate and chromate was. In contrast, only vanadium-containing compounds significantly stimulated prostaglandin (PG) synthesis, and, in fact, selenate significantly inhibited PG production. Finally, only sodium molybdate- and vanadium-containing compounds appeared to increase follicular adenosine 3',5'-cyclic monophosphate content. While all oxoanions stimulated in vitro ovulation, they had differential effects on certain signal transduction pathways when tested at concentrations that stimulated in vitro ovulation. From the results, two basic groups could be delineated, one containing tungstate-, molybdate-, and vanadium-containing compounds and the other selenate and chromate. Thus the mechanism by which ovulation is induced by chromate and selenate may be different from that of vanadium-containing compounds, molybdate, and tungstate.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗

Evidence for an inhibitory dopaminergic and stimulatory noradrenergic hypothalamic influence on PMS-induced ovulation in the immature rat. II. A pharmacological analysis.

Pregnant mare's serum gonadotropin (PMS; 10 IU day 30)-induced ovulation was used as a model to study the effect of drugs interfering with monoamine neuro-transmission on CNS processes controlling ovulation. The drugs were administered during the critical period on day 32 and tubal eggs were counted in the morning of day 33. When injected during the critical period, dopamine (DA) receptor agonists such as apomorphine, ET 495, ergotamine, 2-bromo-alpha-ergocryptine, lergotrile and ergocornine inhibited ovulation, an effect which was counteracted by the DA receptor blocking agent, pimozide. However, by itself pimozide had no significant effect, whereas combined noradrenaline (NA) and DA receptor blocking agents such as chlorpromazine and clozapine inhibited ovulation. alpha- and beta-adrenergic blocking agents and drugs influencing 5-hydroxytryptamine (5-HT) neurotransmission did not affect ovulation. LH-RH removed the ovulatory blockade induced by ET 495 in the same dose-range as it removed pentobarbital-induced blockade of ovulation. Furthermore, ergocornine did not black ovulation after the critical period and was less effective when given prior to the critical period. Therefore it is likely that the DA receptor agonists act via a central action. Thus, the present findings give further support for the existence of a central inhibitory DA and facilitory NA mechanism in the control of PMS-induced ovulation in the immature female rat.

Animals↗

Counteraction of the haloperidol blockade of ovulation by bromocriptine, and the effect of bromocriptine on LH and prolactin secretion.

Previous experiments showed that haloperidol (Haldol) blocked LH release and ovulation when injected on the day of proestrus in the female rat. The present studies were designed to investigate the mechanism of Haldol blockade and the possibility that bromocriptine (CB) might counteract the effect. One hour prior to subcutaneous injection of an effective dose of Haldol (0.25 mg/kg at 09.30 h), CB was injected intraperitoneally at one of four doses (2.5, 5.0, 7.5, or 10.0 mg/kg at 08.30 h). Bromocriptine was effective at restoring LH release and ovulation, and the optimal dose for this particular experiment was found to be 7.5 mg/kg. The highest dose (10.0 mg/kg), however, resulted in no significant increase in ovulation. Treating animals with CB (5.0, 10.0, or 20.0 mg/kg at 08.30 h) followed by control vehicle showed that high doses of CB caused a significant inhibition of LH release and ovulation. After 20.0 mg/kg there was no significant surge of LH, and although ovulation did occur it was significantly suppressed when compared to control animals (p = 0.017). These results showed that appropriate doses of CB counteract the Haldol blockade of LH release and ovulation. The suppression of Haldol-induced PRL secretion by low-dose CB, without the significant restoration of ovulation, supported the hypothesis that the Haldol blockade was mediated via a direct effect of Haldol on central nervous system control mechanisms. While CB alone exerted a profound inhibition of PRL at low doses, it had no effect on LH release. CB at high doses, however, was inhibitory to both LH release and ovulation.

Animals↗

The effects of a gonadotropin-releasing hormone agonist on ovulation and steroidogenesis during perfusion of rabbit and rat ovaries in vitro.

The ability of a GnRH agonist (GnRHa) to exert direct effects on rat and rabbit ovaries was examined in vitro. Ovaries of estrous rabbits and immature, PMSG-primed rats were surgically removed and perfused with a defined medium via an aortic cannula. In this system, the ovary remains viable and capable of undergoing ovulation in response to LH. Samples of perfusion medium were taken for steroid measurements and the number of ovulations determined by direct observation (rabbit) or oocyte recovery (rat). Follicles of ovaries perfused with medium alone rarely ovulated. GnRHa (0.1 micrograms/ml) induced ovulations in 6 of 7 rat ovaries (4 to 22 ovulations per ovulating ovary) and this effect was blocked by a GnRH antagonist. In contrast, a much higher dose of the agonist (10 micrograms/ml) induced ovulations in only 7 of 15 rabbit ovaries. GnRHa caused small but significant increases in progesterone levels in the perfusion medium in both species in comparison to no treatment. Mean estradiol levels also tended to be higher in the GnRHa groups in comparison to controls but the differences were not significant. GnRHa appears to act directly on both the rabbit and rat ovary but the rat ovary is much more sensitive to its ovulation-inducing effects.

Animals↗

Inhibitors of mammalian tissue collagenase and metalloproteinases suppress ovulation in the perfused rat ovary.

We have examined the effects of a new synthetic inhibitor of mammalian tissue collagenase, CI-1 (N-[3-N-(benzyloxycarbonyl)amino-1-(R)carboxypropyl]L-leucyl-O-methyl-L- tyrosine N-methylamide; G. D. Searle SC 40827), and a general metalloproteinase inhibitor, 1,10-phenanthroline, on ovulation, as judged by the observation of follicular rupture, and on progesterone production of the perfused rat ovary. Ovaries of PMSG (20 IU)-primed rats were perfused for 21 h, and samples of medium were taken for analysis of progesterone concentration. The number of ovulations was estimated by counting the number of oocytes released into the perfusion chamber. Ovaries were stimulated with LH (0.1 micrograms/ml) plus 3-isobutyl-1-methylxanthine (IBMX; 0.2 mM), and this treatment resulted in a mean of 17.2 ovulations/treated ovary. 1,10-Phenanthroline dose-dependently inhibited ovulation, with 0, 0.2, and 12.5 ovulations/treated ovary at 1.0, 0.1, and 0.01 mM, respectively. This inhibition of ovulation closely paralleled the inhibition of extracted collagenase from uterus and ovary. However, 1,10-phenanthroline also suppressed progesterone release in a dose-dependent manner. Addition of the collagenase inhibitor (CI-1; 25 microM) 1 h after LH plus IBMX inhibited ovulation (6.3 ovulations/treated ovary). Its relatively inactive stereoisomer (CI-2; 25 microM) did not suppress ovulation (20.0 ovulations/treated ovary). CI-1 inhibited extracted uterine collagenase 50% at a concentration of 2 microM, whereas CI-2 was only 1/15th as effective. There was an 80% loss of CI-1 from the medium during the perfusions. Neither CI-1 nor CI-2 had any effect on LH plus IBMX-stimulated progesterone release. These data demonstrate that the general metalloproteinase inhibitor 1,10-phenanthroline is able to inhibit ovulation, but also inhibits steroidogenesis. The more specific inhibitor of collagenase, CI-1, can inhibit ovulation without affecting steroid production. These data indicate an important role for collagenase in the ovulatory process.

1-Methyl-3-isobutylxanthine↗

Induction of ovulation by LH and FSH in the presence of antigonadotrophic sera.

Surges of both LH and FSH are secreted on the day of proestrus in the rat; both surges are blocked by pentobarbital (PB), WHICH ALSO BLOCKS OVULATION. The purposes of the present study were (a) to see if antisera to ovine LH or FSH would prevent ovulation from endogenously secreted rat hormones; (b) to see if exogenous ovine LH or FSH alone can cause ovulation in the presence of antiserum to ovine LH or FSH, when endogenous hormone secretion is suppressed by PB. Antisera were assessed for anti-OAAD or anti-hCG augmentation activity against ovine and/or rat pituitary hormones. (a) With respect to tests against endogenously secreted hormones, antisera to LH block ovulation, but antisera to FSH do not, regardless of their potency against exogenous hormones. (b) Antisera to either ovine LH or FSH can prevent ovulation to either exogenous ovine hormone, in relation to their ability to block LH on OAAD bioassay, but not in relation to their ability to block FSH on the hCG augmentation test. However, one antiserum to FSH, which had very low anti-OAAD activity,was able to prevent ovine FSH, but not ovine LH, from causing ovulation, suggesting that not all of the ability of exogenous FSH to cause ovulation is related to intrinsic or contaminating OAAD activity. These data suggest that LH (as defined by OAAD) is the obligatory ovulating hormone in the rat. Additional data on uteirine intralumenal water in the presence of PB blockade indicate that LH, but not FSH, can induce some estrogen secretion, but that either hormone may cause some progesterone secretion.

Animals↗

Fertility, ovulation and maturation of eggs in mares injected with HCG.

Pony mares were observed from January to August for incidence of oestrus, duration of oestrus, length of the oestrous cycle and for ovulation and fertility after injection of HCG. From January to 15 May most mares showed oestrus but the duration of oestrus was quite variable and few mares ovulated in response to HCG. From 15 May to 17 August oestrous cycles were more regular and ovulation was induced within 40-50 h by an intramuscular injection of 1500-5000 i.u. HCG. Pregnancy was established by one mating at a fixed time after HCG in 20 of 69 mares. Degenerate eggs were recovered from the oviducts of anoestrous recently ovulated, mated, unmated and pregnant mares. The first polar body was formed before ovulation in 2 eggs and had not formed in 2 recently ovulated eggs flushed from the oviduct. The second polar body formed after sperm penetration 10-12 h after ovulation. After formation of pronuclei, the first cleavage division occurred at 20 h and the second at 32 h after ovulation. Oestrus was inhibited by progesterone administered by vaginal devices but occurred within 1-3 days in 12 of the 20 mares after withdrawal of the devices.

Animals↗

Semen-induced ovulation in the bactrian camel (Camelus bactrianus).

Bactrian camels (63 female female, 8 male male) were used in the breeding season to determine the factors that will induce ovulation. After insemination of semen samples into the vagina, the ovaries were checked for ovulation by rectal palpation. The results indicated that ovulation was induced by the seminal plasma, but not by the spermatozoa, and the incidence of ovulation after insemination was 87%. Most of the females (66%) had ovulated by 36 h after insemination and the rest by 48 h, as after natural service. The least amount of semen required to elicit ovulation was about 1.0 ml. Intramuscular injections of LH, hCG and LHRH also caused ovulation, even in females that had not ovulated in response to insemination.

Animals↗

Effects of monoclonal antibody against PMSG administered shortly after the preovulatory LH surge on time and number of ovulations in PMSG/PG-treated cows.

Normally cyclic heifers received 2500 i.u. PMSG i.m. at Day 10 of the oestrous cycle and 15 mg prostaglandin (PG) i.m. 48 h later. From 30 h after PG the LH concentration in the peripheral blood was estimated every hour using a rapid RIA method which allowed the LH concentration to be known within 4 h. Monoclonal antibody against PMSG was injected in the jugular vein of 29 heifers at 4.8 h after the maximum of the preovulatory LH peak; 28 heifers were not treated with anti-PMSG (controls). Peripheral blood concentrations of PMSG, LH, progesterone and oestradiol were compared. Ovaries were collected by ovariectomy at fixed times, 22-30 h after the LH peak, and numbers were counted of small (2-10 mm), large (greater than 10 mm) and ovulated follicles, and of follicles with a stigma. In anti-PMSG-treated cows, the PMSG concentration fell sharply to non-detectable levels within 2 h of the treatment, indicating that PMSG was neutralized in these cows at the onset of final follicular maturation. In all cows, the concentration of oestradiol showed a significant decrease at about 8 h after the LH peak. After anti-PMSG treatment ovulations took place from 24 until 30 h after the LH peak, whereas in control cows follicles had already ovulated at or before 22 h and ovulations continued until 30 h. At 30 h 90% of the follicles had ovulated in anti-PMSG-treated cows vs 72% in the controls, resulting in 15 and 8 ovulations per cow respectively (P less than 0.05). Also, administration of monoclonal antibody against PMSG synchronized final follicular maturation and shortened the period of multiple ovulations. In conclusion, neutralization of PMSG shortly after the preovulatory LH peak suppresses adverse effects of PMSG on final follicular maturation, leading to an almost 2-fold increase of the ovulation rate.

Animals↗

LH receptor induction and ovulation rate in mice selected for litter size and body weight.

Female mice from lines which had undergone long-term single trait and antagonistic index selection for litter size and body weight were analysed for ovulation rate and LH receptor induction. Compared to randomly selected controls, selection for large litter size increased ovulation rate (60%; P less than 0.001) and decreased LH receptor induction per microgram ovarian DNA (87%; P less than 0.01). Selection for large body weight increased ovulation rate (18%; P less than 0.001), but did not lead to a significant correlated response in LH receptor induction. Index selection for large litter size and small body weight increased ovulation rate (14%; P less than 0.01) and decreased LH receptor induction (72%; P less than 0.01), while index selection for small litter size and large body weight did not significantly alter either ovulation rate or LH receptor induction. LH receptor quantities in testes of males from the 5 lines did not exhibit the among-line profile which was observed in ovaries of females. These results confirm the role of ovulation rate in mediation of the positive genetic correlation between litter size and body weight in mice. Increased ovulation rate in mice selected for large litter size may be due to mechanisms associated with LH receptors as well as factors related to growth. In contrast, increased ovulation rate in mice selected for large body weight may be due exclusively to factors related to growth.

Animals↗