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Department of Obstetrics and Gynecology, Center for Reproductive Biology, University of Edinburgh (C.J.H.S., B.K.C., D.T.B.), Edinburgh, United Kingdom EH3 9EW; and the Division of Development and Reproduction, Roslin Institute (Edinburgh) (R.W.), Roslin, Midlothian, United Kingdom EH25 9PS
Address all correspondence and requests for reprints to: Prof. David T. Baird, Department of Obstetrics and Gynecology, Center for Reproductive Biology, University of Edinburgh, 37 Chalmers Street, Edinburgh, United Kingdom EH3 9EW. E-mail: mh{at}med.srv1.ed.ac.uk
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Abstract |
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The ovarian secretion of dimeric inhibin A was investigated and related to the secretion of ovarian steroids, the concentration of gonadotropins, and the pattern of ovarian follicular development during the follicular and early luteal phases in ewes with an ovarian autotransplant with or without the FecB gene.
The secretion of inhibin A was related to the presence of large estrogenic follicles, being high during the follicular phase and falling after the LH surge (P < 0.05) before increasing during the early luteal phase (P < 0.05). There were no differences in the timing of the onset of the LH surge, the concentrations of FSH and progesterone, or the rates of inhibin A, estradiol, and androstenedione secretion during the follicular or luteal phase between ewes with and without the Booroola gene. Although the overall pattern of follicular development was similar between the genotypes, the ovulation rate was higher (P < 0.05) in the gene carrier ewes, and the ovulatory follicles and corpora lutea were significantly smaller (P < 0.05) than those in noncarrier animals. During the luteal phase, the diameter of the large follicles from the first wave was smaller (P < 0.05) in the gene carrier than in noncarrier ewes.
Because there are no qualitative or quantitative differences in the pattern of secretion of pituitary gonadotropins or ovarian hormones between the two genotypes, we conclude that is likely that the FecB gene exerts its action at the level of ovary.
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The development of antral follicles is dependent on the action of
gonadotropins, primarily FSH (6, 7), the secretion of which is
controlled by the interaction of estradiol and inhibin, both products
of ovarian follicles, in a feedback loop on the pituitary (8). Although
there is substantial experimental evidence, both in vivo (9, 10) and in vitro (11, 12), that inhibin plays an important
role in the regulation of FSH secretion in the sheep, the pattern of
secretion of dimeric inhibin in blood is less clear due to limitations
in the assays employed for its measurement. Most of the available RIAs
rely on antibodies raised against purified or synthetic fragments of
the 
-subunit and are unable to discriminate between dimeric inhibins
and a range of nonbioactive forms of the -subunit; they measure what
has become known as immunoreactive inhibin (13). Although bioassays are
able to measure the active forms of inhibin, they are susceptible to
interference by other factors, notably the ovarian steroids (13).
Bioassays cannot distinguish between the two forms of inhibin (inhibin
A and inhibin B) that appear to have different biopotencies (14) and
different patterns of secretion during the cycle (15, 16). During the
menstrual cycle, inhibin B is high during the early follicular phase
and is associated with the presence of small follicles, whereas inhibin
A is associated with the presence of large estrogenic follicles, being
low at the beginning of the follicular phase and increasing before
ovulation before a further increase again to the highest levels during
the luteal phase (15, 17).
There have been few reports on the pattern of secretion of dimeric inhibin A in sheep, and despite intensive study, the temporal relationship between follicular development and changes in the concentration of gonadotropins and ovarian hormone secretion in ewes carrying the FecB gene are not well characterized. In this study we investigated the effect of the Booroola gene on the secretion of inhibin A and ovarian steroids, the concentration of gonadotropins, and dynamics of follicular development during the follicular and early luteal phases of the estrous cycle in ewes with an ovarian autotransplant. This preparation permits the collection of repeated samples of ovarian venous blood in conscious animals and facilitates determination of the ovarian follicle population by high resolution ultrasound.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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(125 µg, im; Estrumate, Cooper’s Animal Health,
Crewe, UK) given 17 days apart. The day before the start of blood sampling, the jugular and ovarian veins were cannulated under local anesthesia as previously described (20). The ewes were placed in metabolism crates and received a prophylactic treatment of broad spectrum, long acting antibiotic (3 ml, im; Clamoxil, SmithKline Beecham, Surrey, UK) every 3 days throughout the experiment.
Blood sampling
Samples of ovarian (7 ml) and jugular (3 ml) venous blood were
collected at 6-h intervals for 10 days starting on the day before
induction of luteal regression with the second cloprostenol injection.
Ovarian blood flow on every sample was measured by timing the
collection of ovarian venous blood, and hormone secretion rates were
calculated after correcting for the hematocrit (21). After sampling,
each cannula was flushed with 5 ml of a solution of 250 IU sodium
heparin/ml isotonic saline. The blood was centrifuged at 4 C, and the
plasma was separated and stored at -20 C until assay.
In addition, three periods of intensive blood sampling were carried out at the following times: 1) late luteal phase, before the second injection of cloprostenol (15-min intervals for 3 h) to evaluate the ovarian response to a GnRH challenge (250 ng in 2 ml sterile saline, iv; Sigma Chemical Co., Poole, UK); 2) early follicular phase, 12 h after the cloprostenol treatment (10-min intervals for 4 h); and 3) late follicular phase, 36 h after the second cloprostenol injection (10-min intervals for 4 h). Ovarian blood flow was measured hourly during periods of intensive blood sampling, with the intervening samples withdrawn by syringe.
Scanning procedure
The skin over the transplanted ovary was clipped and shaved at
the beginning of the experiment and maintained free of wool throughout.
Before each scan, the area was covered with scanning gel (Siel Sound
Gel, Siel Imaging Equipment, Aldermaston, UK). The ovaries were scanned
at 12-h intervals in both horizontal (dorso/ventral) and vertical
(cranio/caudal) planes, using a 7.5-MHz linear transducer (model
UST-5512U-7.5, Aloka, Japan) with a real-time ultrasound scanner
(SSD-500, Aloka). All ultrasound exams were recorded on video cassette
tape for subsequent analysis.
The tapes were played in slow motion, and the image was frozen at the largest section of the antral cavity for each individual follicle greater than 2.5 mm in diameter. The image was digitized into pixels of 256 shades of gray, and using the NIH Image software (http://rsb.info.nih.gov/NIH-Image/download.html), the periphery of the follicle was identified. Measurements were taken for the major and minor axes of the best-fitted ellipsis for each follicle. The diameters of the follicles were determined as a mean of the two axes measured.
Immunoassay
Gonadotropin and steroid plasma concentrations were measured in
duplicate using previously described double antibody RIA. FSH, LH, and
progesterone were determined in unextracted jugular venous samples
(22). Androstenedione and estradiol (22) were measured in ovarian
venous plasma samples after solvent extraction. The sensitivities of
the assay for FSH, LH, progesterone, androstenedione, and estradiol
were 0.3 µg/liter (USDA, oFSH, SIAFP-RP2), 0.2 µg/liter (NIDDK,
oLH, S23), 380 pmol/liter, 175 pmol/liter, and 50 pmol/liter,
respectively. The concentration of inhibin A in ovarian venous plasma
was measured by two-site enzyme-linked immunosorbent assay (ELISA),
described for use initially in human plasma samples (17) and modified
for use in sheep plasma (23). The immunoassay is based on the use of an
immobilized monoclonal antibody (E4) to the ßA-subunit as a capture
antibody, a biotinylated C-specific monoclonal antibody (17329/H2)
as a detection antibody, and immunopurified 32-kDa bovine inhibin in
ovariectomized sheep plasma as standard in the range 15.6–1000 pg/ml.
In contrast to the sheep assay previously described (23) and in common
with the human assay (17), the standards and samples were denatured by
boiling in 6% SDS before oxidation. Standards and samples are
denatured and oxidized before incubation of the assay in a 96-well
dish. The plates were read using Labsystems Multiskan MCC/340 (Life
Science International, Basingstoke, UK) plate reader at a wavelength of
492 nm. The sensitivity of the ELISA was 30 ng/liter, and serial
dilution of ovine follicle fluid gave ELISA response curves parallel to
that of the purified 32-kDa bovine inhibin standard. The intra- and
interassay variations in the immunoassays used were less than 15% in
the ED20–80 range.
Statistical analysis
The data were normalized with respect to two time periods of
physiological significance. The first was the time of cloprostenol
injection (±12 h), and the second related to the onset of the LH
surge, defined as the nadir point before LH concentrations exceed 10
ng/ml (day 0). For analysis of the relationship between the diameters
of the large follicles (that grew to a diameter of at least 4.5 mm)
that developed during the luteal phase and hormone secretion, follicles
were aligned by emergence (first time a follicle was observed in the
scans with a diameter between 2.5–3 mm). When more than one large
follicle or corpus luteum (CL) per ewe was observed, data from all
structures were included to calculate the mean values, but the number
of animals was used to calculate the SEM. The effects of
time on follicular diameter and hormone concentrations between the
genotypes were analyzed by repeated samples ANOVA, using Systat
software (Systat, Evanston, IL). Comparison of the interval
luteolysis-onset LH surge and the ovulation rate between the genotypes
was performed by independent Student’s t test, using the
same software.
The pattern of pulsatile hormone secretion during the intensive blood sampling were determined using Munro pulse analysis software (Zaristow Software, Haddington, UK). The effect of genotype on the number of pulses, amplitude, nadir, and mean concentration during the periods of intensive blood sampling was analyzed by repeated samples ANOVA, using the Systat statistical package.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Pattern of hormone secretion
In all ewes regardless of genotype, the concentration of
progesterone in jugular venous blood declined (P <
0.05) after cloprostenol treatment and remained at basal levels until 4
days after the LH surge, when it started to increase (P
< 0.05) and continued to rise until the end of the sampling period
(Fig. 1
).
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The mean secretion of inhibin A was not different between the genotypes
and, in contrast to the ovarian steroids, remained relatively stable
during the follicular phase. Inhibin A secretion decreased
(P < 0.05) after the LH surge in both genotypes and
increased after day 1, reaching a level of about 4 ng/min on day 3
(Fig. 1
).
There was no significant difference in the concentration or profiles of
FSH between the genotypes (Fig. 1). The concentration of FSH in jugular
venous blood decreased after cloprostenol-induced luteolysis
(P < 0.05) and remained around 1 ng/ml until the time
of the LH surge, when a synchronous FSH peak occurred
(P < 0.05). No discrete second FSH peak was apparent
in the mean data, but these were evident in profiles from individual
animals (Fig. 2). On day 1, FSH levels
fell to their lowest value during the luteal phase (P
< 0.05) and then sharply increased (P < 0.01),
doubling in concentration on day 2, and remaining around 2 µg/liter
for a day before starting to decrease. Although not statistically
significant, FSH tended to decline earlier between days 1–3 in nongene
carriers than in carrier animals.
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). The secretion of
androstenedione and estradiol increased progressively after
cloprostenol injection (P < 0.05) and reached a
maximum at the time of the LH surge (P < 0.05). On day
1 the rate of ovarian steroid secretion had fallen to its lowest value
during the cycle (P < 0.05), subsequently starting to
increase on day 2 (P < 0.05) to plateau on day 3.5
before starting to decline on day 4.5 (P < 0.05).
Pattern of episodic hormone secretion
Mean data for both genotypes during the luteal and early and late
follicular phases on the characteristics of pulsatile LH release and
estradiol and androstenedione secretion are shown in Fig. 3. During the luteal phase, the amplitude
of GnRH-induced LH pulses was similar between the genotypes, but
noncarrier ewes had higher nadir concentrations of LH
(P < 0.05), resulting in increased mean concentrations
of LH in noncarrier ewes. However, the characteristic pulsatile steroid
responses to this LH stimulus were similar between the genotypes
(P > 0.05).
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During the follicular phase, the pulse frequency progressively increased for all three hormones, but there was no effect on the amplitude of the pulses. Neither frequency nor amplitude of ovarian steroids pulses were influenced by the Booroola gene (P > 0.05), but the amplitude of the LH pulses was higher (P < 0.05) in the noncarrier ewes. However, the pulse nadir and mean concentrations of LH, estradiol, and androstenedione were higher (P < 0.05) in the noncarrier ewes 12 h after cloprostenol-induced luteolysis. Thirty-six hours after luteolysis, the pulse nadir and mean concentration of androstenedione remained higher in the nongene carriers (P < 0.05), but the values for LH and estradiol were not different between the genotypes (P > 0.05).
Relationship between follicular development and hormone
secretion
The patterns of follicular growth and hormone secretion are
illustrated in Figs. 1 and 2. The ovulatory follicles in gene carrier
ewes were significantly smaller (P < 0.05) than those
in noncarrier animals and gave rise to CL of smaller diameter
(P < 0.05). The mean diameters of the ovulatory
follicles at the time of injection of cloprostenol were 4.8 ± 0.3
mm (mean ± SEM; n = 5) and 4.0 ± 0.3 mm
(n = 6), 6.0 ± 0.3 and 5.4 ± 0.3 mm at the onset of
the LH surge, and 5.9 ± 0.3 and 5.6 ± 0.3 mm at the time of
estimated ovulation on day 1 in noncarrier and carrier ewes,
respectively. In the early luteal phase, between days 0–4, the
ovulatory follicle/CL doubled in size and were 12.4 ± 0.6 and
10.4 ± 0.4 mm in noncarrier and carrier ewes, respectively. The
CL remained around these diameters during the remainder of the luteal
phase (Fig. 1).
In the early luteal phase of the cycle, all ewes developed at least one
large follicle (Fig. 2). However, the number of large follicles was
significantly higher (P < 0.05) in gene carrier ewes
(mean ± SEM, 3.0 ± 0.4; n = 6) than in
noncarrier animals (1.8 ± 0.2; n = 5). The large follicles
grew in a linear fashion at a rate of 1 mm/day until they achieved a
diameter of around 5 mm on day 3. No further significant changes in
follicle diameter were observed until day 5.5, when the follicles
started to regress (P < 0.05). The concentrations of
estradiol, androstenedione, and inhibin A in ovarian venous blood
increased in parallel with the growth of large follicles in both
genotypes. However, the secretion of steroids decreased
(P < 0.05) before any reduction in the diameter of
large antral follicles.
Dominance in the first wave of follicular development in the luteal
phase
The relationship between follicular development during the first
wave of follicles in the luteal phase and the pattern of gonadotropin
and ovarian hormones in both genotypes is presented in detail in Fig. 4, with the data aligned to the time of
emergence of the large follicles.
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The concentrations of FSH in both genotypes were high at the emergence of the follicles, decreased as the they grew (P < 0.05), and remained low while the large follicles were actively secreting estradiol.
The pattern of ovarian hormones was not influenced by the Booroola
gene. The secretion of ovarian hormone increased as the large follicles
grew, except that the concentration of estradiol did not start to rise
until 1 day after emergence, when the follicles were above 3.5 mm in
diameter (P < 0.05). There was a progressive decline
(P < 0.05) in the secretion of estradiol starting 3.5
days after follicle emergence (Fig. 4). The secretion of inhibin A also
started to decrease at a similar time, but the reduction was of a
lesser magnitude. The first significant decline in large follicle
diameter was not observed until a day later. Therefore, the follicle
persisted as a recognizable structure long after it had become atretic
and had ceased to be a significant source of steroid secretion.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The association of inhibin A secretion and large antral follicles is
consistent with the observation in women that the concentrations of
inhibin A are higher in the late follicular phase after selection of
the large follicle (17). Similarly, in the rat, inhibin A is at its
highest concentration during proestrus, concomitant with the selection
of large follicles (16). The secretion of dimeric inhibin was
constantly high during the follicular phase and was similar to the
pattern of immunoreactive inhibin reported previously in sheep (22, 24), but the drop in inhibin A observed after the LH surge differs from
the findings of previous studies in which a maintenance or increase in
immunoreactive inhibin secretion was observed (22, 24). The pattern of
secretion of inhibin A is consistent with the lack of messenger RNA
expression for both - and ßA-subunits of inhibin in large antral
follicles during and after the LH surge (25) and the observation that
the highest rate of atresia of follicles over 1 mm in diameter is found
on day 1 of the estrous cycle (26). The difference in the pattern of
secretion between immunoreactive inhibin and dimeric inhibin A could
reflect the release of free -subunit from the follicular fluid at
ovulation (22). Inhibin A secretion increased progressively during the
early luteal phase contemporaneously with the emergence of the large
follicles. However, it did not show the sharp decrease in secretion
observed for the ovarian steroids at the end of the first follicular
wave, suggesting that although inhibin A is secreted mainly by the
large follicles, other antral follicles make a significant contribution
toward overall ovarian secretion (27, 28), a conclusion supported by
recent in vitro studies showing that sheep granulosa cells
from small follicles secrete significant quantities of inhibin A
(29).
The most consistent characteristic of ewes carrying the Booroola gene is a large number of ovulatory follicles that are smaller than those from the noncarrier animals (2, 3, 30). In the present experiment using serial measurements of individual follicles we confirmed these observations and, in addition, observed that there were more follicles present during the first wave of follicular development of the luteal phase in the gene carrier ewes and they matured at a smaller size than those in the noncarrier animals. These observations are consistent with what has been previously demonstrated in vitro that in ewes carrying the Booroola gene the peak in granulosa cell proliferation (measured by mitotic index) occurs in follicles of smaller diameter (30). Further, follicles from gene carrier ewes also exhibit precocious differentiation of granulosa cells, with LH receptor (31), gonadotropin-stimulated cAMP production (32, 33), and aromatase activity (32, 34) occurring at a smaller follicle size than in follicles from noncarrier ewes.
The overall pulsatile pattern of LH, androstenedione, and estradiol during the luteal and follicular phases was not influenced by the presence of the Booroola gene, with the frequency of pulses increasing progressively during the follicular phase in a pattern similar to that observed in other breeds of sheep (35). However, there were differences between genotypes in some characteristics of the pulsatile secretion of LH and steroids. The most consistent differences were lower LH and steroid pulse nadirs, which led to lower overall levels of LH and steroid secretion in the carrier ewes, particularly during the luteal and early follicular phases. These results differ from earlier studies that reported no effect of the Booroola gene on the mean concentration of LH or pulse frequency (36, 37) or consistently higher LH pulse amplitude and concentration in ewes that were homozygous carriers of the Booroola gene throughout the follicular phase (38). We have no explanation for this difference, but the fact that the difference in the ovulation rate is maintained between the genotypes and the responses to GnRH stimulation are similar indicate that the gene action is unlikely to be due to LH.
In this study the secretion of ovarian hormones was not influenced by the Booroola gene, a result that supports previous findings that the secretion of estradiol is similar among the genotypes in ovarian venous blood obtained from anesthetized animals (2, 33, 34) and during short term in vitro cultures of granulosa cells (32, 39, 40). Tsonis et al. (41) reported that the pattern of estradiol secretion at selected intervals during the follicular phase was similar between genotypes of the Booroola gene. The present results extend these observations on steroid secretion, showing that the pattern of ovarian steroid secretion during the follicular and early luteal phases of the estrous cycle is not different between the Booroola genotypes and is similar to those in other breeds of sheep (22, 42). The secretion of dimeric inhibin A was also similar between the genotypes during the luteal and follicular phases, which is in agreement with other reports of the secretion of bioactive inhibin (41) and immunoreactive inhibin (24). These findings are supported by the fact that the FecB gene does not affect the FSH response of ovariectomized ewes to treatment with estradiol or follicular fluid (43) or the response to passive immunization against an inhibin peptide (44).
The fact that FSH concentrations were similar between the genotype groups is contradictory to the findings of a number of studies (37, 38, 45), but is in agreement with those of others (41, 44, 46) and is consistent with the exclusion of linkage with the FecB gene in chromosome 6 and the FSHß gene in chromosome 15 (47). Further, the number and size transcripts of the FSHß gene in pituitary messenger RNA preparations from different genotypes have been found not to be different (47), and there is no genotype difference in the pituitary volume, number of cells, or number and characteristics of gonadotrophs immunostained for FSHß (48). The FecB gene also does not affect the median charge of FSH or its half-life (49). In addition, the fact that the concentrations of FSH were similar in this group of animals before the autotransplant procedure (Campbell, B. K., unpublished observations) precludes the possibility that the lack of difference in FSH was an artifact of the experimental model. The similarity between genotypes in the concentrations of FSH observed in the present study is perhaps not surprising, as the secretion of FSH in sheep is regulated by estradiol and inhibin (8), and the secretion of these ovarian hormones was similar between the genotypes. Thus, higher FSH concentrations do not seem to be essential for the action of the Booroola gene, as the characteristic differences in ovulation rates are maintained when hypophysectomized ewes of different Booroola genotypes are induced to ovulate with standard doses of equine CG and hCG (50). Further, ewes with or without the FecB gene, made hypogonadotropic by GnRH antagonist treatment and stimulated with the same regime of gonadotropins (FSH and LH), maintained the difference in number and follicular/CL size characteristics of the genotypes (51). Together the results suggest that the Booroola gene is likely to act at the level of ovary.
We conclude that the secretion of dimeric inhibin A is related to the presence and emergence of large follicles and is positively associated with estradiol secretion but negatively related to FSH concentration, suggesting that inhibin A is mainly a product of differentiated follicles. The ovulatory follicles and corpora lutea are smaller but greater in number in ewes carrying the FecB gene, resulting in similar secretion of androstenedione, estradiol, and dimeric inhibin A and identical concentrations of FSH. The large follicles that emerge in the first wave of follicular development of the luteal phase also mature at a smaller diameter, suggesting that the Booroola gene acts at an ovarian level modulating gonadotropic signals during both the follicular and early luteal phases of the cycle.
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Acknowledgments |
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Footnotes |
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2 Present address: Department of Agriculture and Horticulture, Sutton
Bonington Campus, University of Nottingham, Loughborough,
Leicestershire, United Kingdom LE12 5RD.
Received June 12, 1997.
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References |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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-ßA dimer) during the oestrous cycle, after
manipulation of ovarian activity and during pregnancy in the ewe. J
Reprod Fertil, in press
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)
and inhibin A (
) and concentration of FSH in jugular venous blood
(
) in two representative animals. A, Typical patterns of a nongene
carrier ewe; B, patterns in an FecB gene
carrier ewe. The dotted line indicates the time of the
onset of the LH surge.
