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Biology of Reproduction 61, 921-926 (1999)
©Copyright 1999 Society for the Study of Reproduction, Inc.

Articles

Corpus Luteum Development and Function in Cattle with Episodic Release of Luteinizing Hormone Pulses Inhibited in the Follicular and Early Luteal Phases of the Estrous Cycle1

J.A. Quintal-Franco3,a, F.N. Kojima4,a, E.J. Melvin5,a, B.R. Lindsey6,a, E. Zanella7,a, K.E. Fike8,a, M.E. Wehrman9,a, D.T. Cloptona, and J.E. Kinder2,a

a Department of Animal Science, University of Nebraska, Lincoln, Nebraska 68583-0908


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The influence of episodic LH pulses before and subsequent to ovulation on size and function of the corpus luteum (CL) in cattle was examined. Treatments were 1) control; 2) LHRH antagonist starting 2 days before the preovulatory LH surge (Antagonist [Ant] -2); 3) LHRH antagonist at initiation of the preovulatory LH surge (Ant 0); and 4) LHRH antagonist starting 2 days after the preovulatory LH surge (Ant 2). Treatments with an LHRH antagonist were continued until 7 days after the preovulatory surge. Diameter of the CL and concentrations of progesterone were monitored during the luteal phase that ensued after treatment. Maximum average diameters of CL were 9.5, 17.5, 21.6, and 28.8 mm for females from the Ant -2, Ant 0, Ant 2, and control groups, respectively (P < 0.01). Compared with those in control animals, concentrations of progesterone in plasma were less (P < 0.01) in animals in which release of LH pulses was inhibited by treatment with antagonist. Arbitrary units under the curve for concentrations of progesterone during the luteal phase of the estrous cycle for Ant -2, Ant 0, Ant 2, and control groups were 19.6, 41.6, 43.6, and 142.2, respectively. There was no difference in circulating concentrations of progesterone (P > 0.1) among antagonist-treated groups. In conclusion, episodic release of LH pulses before, during, and after the time of the preovulatory surge of LH may stimulate development and function of the CL in cattle.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The corpus luteum (CL) is a transient endocrine gland that develops from a graafian follicle after ovulation and is required to support pregnancy in mammals. LH is essential for maintenance of progesterone production by luteal cells of many species. The concept that LH is the main luteotropic hormone in cattle was proposed over three decades ago [1]. In cattle, there is a greater frequency of episodic LH pulses during the follicular phase (~7 pulses per 12 h) as compared with the midluteal phase (~3 pulses per 12 h) of the estrous cycle [2]. In cattle, association between LH pulses and secretion of progesterone indicates that during the midluteal phase of the estrous cycle, LH pulses are followed by a release of progesterone [3]; however, pulses of LH and progesterone secretion are not associated during the early luteal phase [4].

Dependence of luteal function on LH varies during different stages of the estrous cycle and among species [5, 6]. Abolishment of LH pulses by treatment of ewes with an LHRH antagonist on Day 6 of the estrous cycle (Day 0 = estrus) resulted in a slight decrease in concentrations of progesterone in blood, and concentrations remained suppressed until the typical time during the estrous cycle for cessation of luteal function. However, when ewes were treated with an LHRH antagonist on Day 13, progesterone secretion declined rapidly with concurrent regression of the CL. Episodic release of LH pulses is required for CL development but is not required to maintain luteal function in cattle [6]. When episodic release of LH was inhibited by treatment with an LHRH antagonist from Days 2 to 7 or 7 to 12 of the estrous cycle, there was diminished luteal function compared with that in untreated control females [6]. Treatment with LHRH antagonist on Days 12–17 of the estrous cycle, however, did not affect luteal function as determined by concentrations of progesterone in blood plasma [6].

Episodic release of LH pulses before the preovulatory surge of gonadotropins may be important for inducing maturation of the dominant ovarian follicle [7]. Women who were infertile due to luteal phase deficiency had a greater frequency of release of LH pulses during the early follicular phase in comparison to women with typical luteal function [8]. There were, however, fewer LH pulses during the early follicular phase of the menstrual cycle in women with a subfunctional CL than in women with typical luteal function [9]. Normal development and function of the CL, therefore, require a frequency of LH pulses in an optimal range, and deviations from this pattern of LH pulses can be detrimental for development of the structure and function of luteal tissue. There is little information about the role of episodic release of LH pulses during the follicular phase and the periovulatory stages of reproductive cycles on luteal development and function; therefore, the specific objective of the present study was to assess the role of episodic LH pulses before, during, and after the preovulatory surge of LH on development and function of the CL of cattle.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Experimental Protocol

The Institutional Animal Care and Use Committee approved all of the procedures used in this experiment at the University of Nebraska. Postpubertal female cattle of composite breeding (n = 21; 1/4 Hereford, 1/4 Angus, 1/4 Red Poll, 1/4 Pinzgauer; 439.9 ± 12.2 kg of body weight) were used in this study. Estrus was synchronized to a common day with two injections of prostaglandin F2{alpha} (PGF2{alpha}; Lutalyse; Pharmacia & Upjohn, Kalamazoo, MI) given 11 days apart.

To synchronize stage of dominant ovarian follicle development among animals so that dominant follicles would be at the same stage of development at the time of luteolysis, all follicles larger than 5 mm were aspirated by transvaginal procedures [10] 4 days before the second treatment of PGF2{alpha}. Aspiration of follicles was performed using a 5.0-MHz convex array probe with a device attached to guide a needle into ovarian follicles that were aspirated while visualized on a monitor (Aloka 500V Corometrics, Wallingford, CT).

Animals were randomly assigned to one of the following treatments: 1) control (n = 5; 5% mannitol); 2) LHRH antagonist ([6]; N-Ac-D-Nal[2]1,4Cl-D-Phe2,D-Pal[3]3,D-Cit6,D-Ala10-LHRH) starting 2 days before initiation of the preovulatory surge of LH (Antagonist [Ant] -2; n = 6); 3) LHRH antagonist at initiation of the preovulatory LH surge (Ant 0; n = 5); and 4) LHRH antagonist starting 2 days after the preovulatory LH surge (Ant 2; n = 5). LHRH antagonist was administered s.c. every 24 h at 10 µg/kg BW [6] until Day 7 of the estrous cycle to all females in treated groups.

Preovulatory surges of LH were experimentally induced in all animals by the intravenous administration of purified bovine LH (bLH; preovulatory LH surge = Day 0) starting 48 h after the second injection of PGF2{alpha}. Purified bLH, at 200 µg/ml, had activity equivalent to that of standard available preparations (NIH-LH-S1 and LH-G3-226B). Administration of LH according to the protocol started about 24 h before the typical time of the endogenous preovulatory surge of gonadotropins. LH was administered at this time so that the LH surge to induce ovulation and stimulate the initial stages of luteinization would be similar in timing and amount among all animals. Doses of LH were calculated to achieve an initial concentration of 100 ng/ml of plasma (6.17 x 10-5 mg/kg BW) and to maintain a concentration of 50 ng/ml of plasma (3.09 x 10-5 mg/kg BW) with subsequent injections at 20-min intervals for 3 h.

Measurements and Sample Collections

To verify accuracy of exogenous bLH treatment to induce ovulation and initial stages of luteinization, blood samples were collected every 20 min from 2 h before the first bLH treatment to 2 h after the last injection, and samples were subsequently analyzed for concentrations of LH. Ovulation and development of the CL (diameter in millimeters) were monitored by ultrasonography using a 7.5-MHz linear array probe and monitor (Aloka 500V Corometrics) every day until Day 12 of the estrous cycle and every other day until the end of the experiment on Day 28. The day of ovulation was defined as the day when the largest follicle disappeared between two consecutive days of ultrasonographic evaluation of ovarian structures [11]. To quantify concentrations of progesterone in plasma, blood samples were collected every 12 h from the time of the second treatment of PGF2{alpha} until Day 28 or the time of detection of the subsequent behavioral estrus.

Samples of blood for quantitation of progesterone were collected in tubes treated with 30% EDTA (50 µl for 10-ml blood sample) and were centrifuged at 2700 x g for 20 min immediately after collection to minimize degradation of progesterone. Plasma was then harvested and stored at -20°C until assayed for concentrations of progesterone. Samples collected for quantification of LH were allowed to clot at room temperature and then were stored at 4°C for 24 h; they were then centrifuged at 2700 x g for 15 min. Serum was subsequently decanted and stored at -20°C until assayed for concentrations of LH.

RIAs

Concentrations of progesterone in plasma were analyzed by RIA [12]. Assay procedures included use of a monoclonal antibody to P4-11-BSA (Bios-Pacific, Emeryville, CA), progesterone-11{alpha}-hemisuccinate trimethyl ester as radiolabeled tracer, and progesterone (Sigma Chemical Co., St. Louis, MO) as standard. Intra- and interassay coefficients of variation were 8% and 4%, respectively. Concentrations of LH in serum were analyzed by RIA using an antibody against LH (TEA-RaOLH#35), highly purified ovine LH (LER-1374A) as radiolabeled tracer, and NIH-LH-B7 as standard [13]. Intra- and interassay coefficients of variation were 7% and 11%, respectively.

Statistical Analysis

The experiment was a completely randomized design. Maximum diameter (in millimeters) of the CL was analyzed using the General Linear Models procedure of SAS [14], including the fixed effects of treatment and day in the model. Function of the CL was analyzed by estimating the total area under the profile of progesterone concentrations in plasma during the estrous cycle. Total progesterone under the curve (arbitrary units) was evaluated using a mathematical equation to determine area and was analyzed with a General Linear Models procedure of SAS considering treatment as the main effect. Comparisons among treatment least-squared means were performed by orthogonal contrasts.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Treatment with bLH to mimic a preovulatory surge of LH resulted in concentrations of LH in circulation above 50 ng/ml in all females (Fig. 1). Data for mean concentrations of LH in circulation during the 3-h treatment with purified bLH are included in Table 1. Ovulation was successfully induced in 16 females within 48 h after treatment with bLH (untreated control = 5; Ant 2 = 4; Ant 0 = 4; Ant -2 = 3); and three more females (Ant 2 = 1; Ant 0 = 1; Ant -2 = 1) ovulated within 72 h after treatment with bLH. Two females in the Ant -2 group did not ovulate. These females, however, had ovarian follicles 10 mm or greater in diameter that were potentially capable of ovulating when the LH treatment was administered. Average size of the largest follicle at the time of treatment with LH was 11.8 ± 1.0, 9.2 ± 0.4, 10.5 ± 1.6, and 12.8 ± 0.9 for the control, Ant -2, Ant 0, and Ant 2 groups, respectively. Day of detection of the behavioral estrus after time of treatment with LH to induce ovulation was Day 20 ± 1, 29 ± 3, 27 ± 2, and 24 ± 2 in females from the control, Ant -2, Ant 0, and Ant 2 groups, respectively. Day of detection of behavioral estrus was earlier (P < 0.05) in females of the control group than in females in any of the treated groups, and earlier (P < 0.05) in the Ant 2-treated females than in the females of the other two treated groups.



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  		FIG. 1. Concentrations of LH in blood plasma of cattle treated with LHRH antagonist at different times relative to the preovulatory LH surge (Day 0 = day of exogenous LH surge)


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  		TABLE 1. Number of animals that had ovulations from dominant follicles, basal and mean concentrations of LH in blood plasma and area under the profile of progesterone concentration during the luteal phase of the estrous cycle of cattle treated with LHRH antagonist and untreated control females

Maximum diameter of the CL during the luteal phase of the estrous cycle when treatments were administered was greatest (P < 0.01) in untreated control females (28.8 ± 1.2) and smallest in females from the Ant -2 (9.5 ± 0.4) group (Fig. 2). Maximum diameter of the CL in females of the Ant 0 (17.5 ± 0.7) and Ant 2 (21.6 ± 0.8) groups during the luteal phase of the estrous cycle was less than in females of the control group (28.8 ± 1.2) but greater (P < 0.01) than in females of the Ant -2 group (9.5 ± 0.4). There was no difference (P > 0.1) in maximum diameter of the CL among females of the Ant 0 or Ant 2 group during the luteal phase of the estrous cycle when treatments were administered.



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  		FIG. 2. Diameter of the CL in untreated control females and females treated with an LHRH antagonist at different times relative to the time of the preovulatory LH surge (Day 0 = Day of exogenous LH surge); data depicted by lines (for area under the progesterone concentration profile during the estrous cycle) indicated by different letters differ; a–c: P < 0.01

Values for concentrations of progesterone during the luteal phase of the estrous cycle were tested for homogeneity of variances using the Bartlett test. Variances were homogeneous among groups, and transformation of data was not required. Compared with concentration of progesterone (area under the curve) in females from the control group, concentration of progesterone during the luteal phase of the estrous cycle was less (P < 0.01) in females in which LH release was inhibited prior to, during, or after the LH surge (Fig. 3). For females in which LH release was inhibited (starting 48 h before the preovulatory LH surge, or at the time of its initiation, or 48 h afterward) and for the control group, arbitrary units under the curve for progesterone concentrations during the luteal phase of the estrous cycle were 19.6 ± 1.6, 41.6 ± 2.3, 43.6 ± 1.9, and 142.2 ± 9.6, respectively. There was no difference (P > 0.1) in concentrations of progesterone during the luteal phase of the estrous cycle as determined by arbitrary units of progesterone in females of the three groups in which release of LH was inhibited by using LHRH antagonist.



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  		FIG. 3. Mean concentration of progesterone in blood plasma from untreated control females and females treated with an LHRH antagonist at different times relative to the preovulatory surge of LH (Day 0 = Day of exogenous LH surge); control group is different from treated groups, P = 0.01


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The present study is the first to provide evidence that episodic release of LH during the 48 h before the preovulatory surge of LH is important for development of the CL in cattle. Inhibition of LH release for the 48 h preceding the preovulatory surge of LH resulted in development of a CL smaller in diameter than those from females of the control group or from females in which episodic release of LH was inhibited coincident with initiation, or starting 48 h after initiation, of the preovulatory surge of LH. The smaller-diameter CL of females in this group indicates that the episodic release of LH pulses during the period preceding the preovulatory surge of gonadotropins is required for maturation of the follicle to allow for development of a CL of typical size.

Sustained episodic stimulation of ovarian follicles by LH pulses may permit maturation of the follicle before the preovulatory surge of LH [7], and this is consistent with the concept that there is preparation of theca and granulosa cells for luteinization before ovulation of the dominant follicle [15]. This may explain why two females in the Ant -2 group did not ovulate despite having follicles similar in diameter to those of other females that did ovulate. Results from previous studies [8, 9] indicate that abnormal patterns of release of LH pulses during the follicular phase of the menstrual cycle of women (either more or less frequent than normal) result in luteal phase deficiency and infertility. Development of a normal CL may depend on a healthy preovulatory follicle with adequate numbers of granulosa cells before ovulation, granulosa cells capable of synthesizing adequate quantities of progesterone, and adequate populations of LH receptors in the granulosa and theca cells [16]. LH modulates its own receptor population in regulation of luteal function [17]. Inadequate numbers of LH receptors in both granulosa and theca cells due to the absence of LH pulses before the preovulatory surge of LH may account for the smaller luteal structure in females in which release of LH was inhibited 48 h before the LH surge.

Alternatively, the smaller luteal structure of females in which episodic LH release was inhibited starting 48 h before the preovulatory surge of LH could have resulted from altered populations of luteal cells. In cattle and sheep, granulosa cells from ovarian follicles develop into large luteal cells, while small luteal cells are derived from theca cells [18]. Angiogenesis is an important aspect of early development of the CL, but in vitro studies indicate that the angiogenic activity of CL of sheep is not controlled by LH stimulation [19]. Eventually, small luteal cells of thecal origin may differentiate into large luteal cells during the late stages of CL development [20]. During luteinization, there is hypertrophy and hyperplasia of theca cells, which give rise to small luteal cells [21]. Small luteal cells possess functional LH receptors that are involved in regulation of progesterone secretion, but LH receptors in large luteal cells of granulosa origin are not involved in regulation of secretion of progesterone; these large cells secrete large amounts of progesterone in the absence of LH stimulation [22]. It is possible, therefore, that in the absence of release of LH pulses during the late stages of ovarian follicular maturation and early luteal development, small luteal cells do not receive the proper stimulation to secrete progesterone and without LH stimulation are not capable of developing into large luteal cells that secrete greater amounts of progesterone.

Secretion of progesterone from the CL of females in which episodic release of LH was inhibited was also suppressed compared with that of females from the control group. Interestingly, there is decreased frequency of LH pulses during the follicular phase of the menstrual cycle of women with a subfunctional CL [9]. Observations in the present study are also consistent with earlier work in sheep in which induced premature ovulation of dominant ovarian follicles with injections of LH resulted in development of subfunctional CL [23]. Subfunctional CL that developed as a consequence of the early induced ovulation in sheep likely resulted from the truncation of LH support during the final stages of development of the dominant ovarian follicles. In the present study, the exogenous LH mimicking the preovulatory LH surge was administered about 24 h before the time of the endogenous LH surge [24]. Luteinization of the dominant ovarian follicle was, therefore, initiated about 24 h before the typical time of initiation of luteinization by the endogenous preovulatory surge of LH. The dominant ovarian follicles in the present study thus did not have the final 24 h of episodic LH pulse stimulation before initiation of luteinization by the preovulatory LH surge. It is interesting, therefore, that secretion of progesterone by CL of animals in the control group, as well as size of CL, was similar to what is typical after initiation of luteinization by endogenous preovulatory surges of LH, which occur on the average at about 65 h after treatment of female cattle with PGF2{alpha} [24]. However, diameter and function of CL in females of the control group might have been greater than they were in the present study if the ovulatory follicle had been stimulated by the final 24 h of episodic LH secretion before the endogenous preovulatory LH surge.

Data from the present study indicate a dissociation of structural and functional development of the CL in cattle. Function of the CL of females from all groups treated with LHRH antagonist was reduced to the same extent as was the function of CL of females from the untreated control group, but the diameter of the CL was greater in females from the Ant 0 and Ant 2 groups than in those from the Ant -2 group. Episodic LH pulses after the preovulatory LH surge are therefore important for development of a CL of typical size. The present data indicate that LH pulses after the preovulatory surge of LH are necessary for both structural and functional development of the CL in cattle. In sheep, LH has been reported to not stimulate mitogenic activity of mixed sheep luteal cell cultures [19]. The function of LH in regulation of development of the luteal structure is therefore not clearly understood.

In the present study, the diameter of the CL that developed in the absence of episodic LH pulses after the preovulatory surge of LH represented about 60% of the diameter of the CL in control females. However, secretion of progesterone from the CL of females in which episodic LH release was inhibited represented about 25% of that produced by the CL of females from the control group. Inhibition of release of LH pulses in females from Days 2 to 12 of the estrous cycle had an effect on function of the CL resulting in a decrease of about 50% in secretion of progesterone compared with values for control females [6]. Effects of the LHRH antagonist in inhibiting release of LH pulses likely extended over a period beyond cessation of treatment. When females are treated with LHRH antagonist from Days 2 to 7 of the estrous cycle, pulse frequency of LH is diminished for up to 10 days after cessation of treatment due to a residual effect of the antagonist [6]. Those results were confirmed with the observations of the delayed time to return to estrus subsequent to treatment in the present study.

The possibility cannot be discounted that the LHRH antagonist may have effects directly at the ovary to inhibit development of the CL. The latter possibility is not likely, however, because contrary to the situation in human and rat ovaries [25], in which the gene for LHRH receptor is expressed, this gene is not expressed in the CL of cattle [26]. Apparently the gene encoding for LHRH, however, is expressed in cumulus-oocyte complexes of cattle [27].

LHRH can be involved in regulation of FSH secretion in some physiological states, and FSH has been reported to have a cooperative luteotropic function with LH in hamsters [28]. Suppression of FSH secretion may, therefore, have contributed to the suppressed luteal function of the treated females as compared with luteal function of the control females in the present study. In females treated with the LHRH antagonist from Days 2 through 7 of the estrous cycle in a previous study, concentrations of FSH between Days 2 and 12 of the estrous cycle were not different from those of untreated control females [29]. In the present study, concentrations of FSH from Days 2 through 12 of the estrous cycle in females treated with LHRH antagonist from Days 2 through 7 (data not reported) were also not different from those of control females. There was suppressed luteal function in both the previous [6] and present studies of females treated with LHRH antagonist from Days 2 to 7 of the estrous cycle as compared with untreated control females in the absence of suppressed concentrations of FSH in blood. It is therefore assumed that LHRH antagonist-induced modulations of FSH concentrations cannot explain why luteal function is suppressed in cattle treated with the LHRH antagonist during the period of luteal development.

In summary, inhibition of release of episodic LH pulses from 2 days before the preovulatory surge of LH until Day 7 of the estrous cycle had the greatest inhibitory effect on development of a CL. Similarly, diameter of the CL was decreased as a result of inhibition of LH release starting at the time of and 2 days after the preovulatory surge of LH up to Day 7 of the estrous cycle. Concomitantly, function of the resulting CL was suppressed by inhibition of LH release at different times relative to the preovulatory surge of LH, as evidenced by reduced capacity to secrete progesterone.

In conclusion, final maturation of the preovulatory follicle may be dependent on episodic release of LH pulses during the last 48 h before the preovulatory surge of LH, and it is required for development of a CL of typical diameter and function in cattle. Episodic release of LH pulses subsequent to the preovulatory surge of LH is also required for development of the CL in cattle. The relatively large amounts of LH released during the preovulatory surge of LH are not sufficiently luteotropic to support secretion of progesterone similar to that of a normal CL. Theca, granulosa, and luteal cells require episodic stimulation by LH pulses during the periovulatory stages of the estrous cycle for development of a luteal structure with typical diameter and steroidogenic capacity in cattle.


   ACKNOWLEDGMENTS
 
We thank Dr. Jerry Reeves for LH antisera; Dr. Leo Reichert Jr. for purified LH; Candy Toombs and Machele Miller for their superb technical assistance with the RIAs; and Karl Moline, Jeff Bergman, and Bob Browelit for their assistance with caring for the cattle.


   FOOTNOTES
 
1 Published as paper 12411, Nebraska Agricultural Research Division. This work was supported by appropriated funds from the State of Nebraska. Back

2 Correspondence: James E. Kinder, 110B Animal Sciences, The Ohio State University, Columbus, OH 43210-1095 FAX: 614-292-2929; kinder.15{at}osu.edu Back

3 Current address: INIFAP-SAGAR. C.E. Moccocha, Apdo. Postal 100 Suc. Merida, Yucatan, Mexico CP-97200. Back

4 Current address: Department of Animal Science, University of Missouri, Columbia, MO 65211. Back

5 Current address: Bowman Gray School of Medicine, Wake Forest University, Winston Salem, NC 27106. Back

6 Current address: Stroud Veterinary Embryo Services, 6601 Granbury Highway, Weatherford, TX 76087. Back

7 Current address: EMBRAPA, Suinos e Aves, Concordia-SC, Brasil. Back

8 Current address: 1713 Linden Road, Harlan, IA 51537. Back

9 Current address: Trans Ova Genetics, Chillicothe, MO 64601. Back

Accepted: May 10, 1999.

Received: October 26, 1998.


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 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
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