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BOR - Papers in Press, published online ahead of print April 2, 2003.
Biol Reprod 2003, 10.1095/biolreprod.102.013821
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BIOLOGY OF REPRODUCTION 69, 398–403 (2003)
DOI: 10.1095/biolreprod.102.013821
© 2003 by the Society for the Study of Reproduction, Inc.

Ovary

Chronic Treatment with an Agonist of Gonadotropin-Releasing Hormone Enhances Luteal Function in Cattle1 ,2

T.L. Davis3,6,7, M.L. Mussard4,6,7, H. Jimenez-Severiano5,6, W.J. Enright8, and J.E. Kinder2,6,7

Department of Animal Sciences,6 University of Nebraska, Lincoln, Nebraska 68583-0908 Department of Animal Sciences,7 Ohio State University, Columbus, Ohio 43210-1095 Intervet International,8 5830 AA Boxmeer, The Netherlands


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Our hypothesis was that luteal function, as determined by plasma progesterone concentrations, and corpus luteum (CL) size is enhanced in cattle administered an agonist of GnRH when the CL is developing as compared with administration of an agonist when the CL is fully functional. Cattle were chronically administered a GnRH agonist, azagly-nafarelin, from Day 3 to Day 21 (D3) or Day 12 to Day 21 (D12) or served as untreated control females (Day 0 = behavioral estrus). Blood samples were serially collected on Days 7 and 14 to evaluate LH secretory patterns and twice daily to measure plasma progesterone. Ultrasonographic examinations were conducted daily to record the area of the CL. CL size and plasma progesterone concentrations were both enhanced in the D3 group as compared with the control group. Progesterone was increased in the D12 group on Days 16 and 17 as compared with the control females. Treatment with GnRH agonist increased basal and mean LH concentrations in both D3 and D12 groups as compared with the controls. We rejected our hypothesis because chronic administration of a GnRH agonist increased plasma progesterone when administered both when the CL was developing and when it was fully functional. The enhanced luteal function was likely due to increased basal LH.

corpus luteum, gonadotropin-releasing hormone, luteinizing hormone, progesterone


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Chronic administration of a GnRH agonist to many species, including rats [1], dogs [2], and humans [3, 4], impairs reproductive function. In domestic ruminants, there is a differential response of pituitary and gonadal function to chronic administration of a GnRH agonist. Chronic treatment of rams with a GnRH agonist suppresses LH, FSH, and testosterone secretion [5, 6]. In contrast, chronic administration of a GnRH agonist enhances pituitary and gonadal function in bulls [7, 8]. The enhanced testicular function [9] is likely attributed to increased basal LH secretion [10].

Treatment of cattle with GnRH or a GnRH agonist has opposing effects on luteal function, depending on the dose, route of administration, and days of the estrous cycle when treatment is administered. For example, injections with various doses of GnRH or GnRH agonist on Day 0 (behavioral estrus) of the estrous cycle increase serum progesterone concentrations during the subsequent luteal phase [11]. Intrauterine infusions of GnRH on Days 12, 13, and 14 did not increase plasma progesterone during the luteal phase [12], whereas s.c. injections of GnRH agonist four times daily from Day 9 through Day 12 of the estrous cycle of cattle increased progesterone concentrations during the luteal phase following treatment and lengthened the estrous cycle [12]. Administration of GnRH on Days 2 and 8 did not affect serum progesterone concentrations during the luteal phase of the estrous cycle [13]. Yet, when cows were treated with GnRH on Days 2 and 8 and the corpora lutea (CL) were collected on Day 10, there was a significant increase in basal progesterone production by bovine luteal slices in vitro [13]. Luteal function is enhanced in cattle treated with GnRH agonist on Day 5 of the estrous cycle [14, 15], possibly because of the accessory CL formed [14, 15] as a result of the acute increase of LH after administration of GnRH. Cows implanted with GnRH agonist from Day 2 through Day 25 had greater concentrations of plasma progesterone than did cows implanted from Day 2 through Day 5, and no accessory CL developed in either group (unpublished results).

LH is the primary luteotropin that supports CL development and maintenance of normal luteal function required for establishment and maintenance of pregnancy [16]. In cattle, LH is released from the anterior pituitary in a pulsatile manner concomitant with the pulse frequency of GnRH from the stalk median eminence [17]. An acute increase of LH can be induced by administration of GnRH agonist, and LH remains elevated for approximately 24 h before returning to basal concentrations [7, 18, 19]. For the duration of the GnRH agonist treatment period, LH concentration is maintained at or slightly greater than basal values, even though pulsatile release of LH is suppressed in cattle treated chronically with GnRH agonist [7, 18, 19]. In cattle, CL development appeared to be dependent on pulsatile release of LH from Day 2 to Day 12 but not after Day 12 of the estrous cycle [20]. Our hypothesis was that luteal function and CL size are enhanced in cows when treatment with the GnRH agonist begins on Day 3 but not when treatment begins on Day 12 of the estrous cycle.


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

The Institutional Animal Care and Use Committee at the University of Nebraska approved all of the procedures used in this experiment. The Food and Drug Administration approved the administration of the GnRH agonist under INAD 10021. Nonlactating cows (n = 26) of composite breed type and similar body condition score (1/4 Hereford, 1/4 Black Angus, 1/4 Pinzgauer, 1/4 Red Poll; 2–11 years of age; 470.8 ± 14.2 kg body weight) were synchronized to a common day of estrus (Day 0 = behavioral estrus) with two i.m. treatments of prostaglandin F2{alpha} (25 mg Lutalyse; Pharmacia and Upjohn Co., Kalamazoo, MI) 11 days apart. Cows were observed for behavioral estrus three times daily beginning 48 h after the second treatment. Intact and short-term (~2 mo) unilaterally ovariectomized cows were utilized in this study. These cows were assigned to one of three treatment groups: untreated controls (Cont; n = 7), Day 3 GnRH agonist (D3; n = 7), or Day 12 GnRH agonist (D12; n = 7). Each treatment group contained similar numbers of intact (Cont, n = 3; D3, n = 3; D12, n = 2) and unilaterally ovariectomized (Cont, n = 4; D3, n = 4; D12, n = 5) cows. GnRH agonist was administered beginning either Day 3 (D3) or Day 12 (D12), and administration continued through Day 21 of the estrous cycle.

Administration of GnRH Agonist

Cows were administered an agonist of GnRH (azagly-nafarelin, [D-Nal(2)6, aza-Gly10] GnRH; Intervet International B.V., Boxmeer, The Netherlands) at a dose of 1 µg kg body weight-1 day-1 using Alzet osmotic pumps (Alza Corp., Palo Alto, CA). Azagly-nafarelin was dissolved in 0.15 M NaCl (VWR Brand, West Chester, PA). The 28-day 2ML4 osmotic pump with a mean pumping rate of 2.6 µl/h was utilized for the D3 treatment group. Cows in the D12 treatment group were administered agonist with the 14-day 2ML2 osmotic pump model with a mean pumping rate of 4.75 µl/h. Filled pumps were incubated at 37°C overnight (prior to implantation into cows) in 0.15 M NaCl to initiate delivery of agonist at the onset of insertion into cows. Osmotic pumps were inserted s.c. using a local anesthetic (lidocaine) near the seventh rib on Day 3 (D3 group) or Day 12 (D12 group) and were removed using a local anesthetic on Day 21 from cows in both treatment groups.

Ultrasonography

One day prior to administration of GnRH agonist (D2 and D11), ovarian follicles >4 mm in diameter were aspirated using an ultrasonographically guided needle [21, 22]. Follicular aspirations were performed with a 17-ga needle guided transvaginally by a 5.0-MHz convex-array transducer and observed on an Aloka 500 V ultrasonographic monitor (Corometrics, Wallingford, CT). Ovarian follicular aspirations were performed to prevent luteinization or ovulation of large follicles that were present on the ovaries and were responsive to the acute increase of LH at administration of the GnRH agonist. Therefore, an increase of plasma progesterone concentrations would be attributed to the GnRH agonist treatment affecting the function of the existing CL and not an induced CL. Ovaries were examined daily with real-time ultrasonography and the ultrasonographic monitor with a 7.5-MHz transrectal linear probe (Corometrics) beginning on Day 1 to measure CL area (cm2) and map follicular development. An estimated value for luteal area was determined at the time of ultrasonography using the built-in area measurement function.

Blood Sampling

Luteal function was assessed by plasma progesterone concentrations during the estrous cycle. Twice daily jugular blood samples were collected in tubes containing 30% EDTA (50 µl for 10-ml blood sample; J.T. Baker, Phillipsburg, NJ) and immediately placed on ice to prevent degradation of steroids. Samples were centrifuged at 1500 x g for 15 min within 2 h of blood collection, and plasma was collected and frozen at -20°C until assayed for progesterone. Blood samples were collected every 20 min for 16 h on Day 7 (Day 7.1 ± 0.2; range, Days 5–8) and Day 14 (Day 14.1 ± 0.2; range, Days 12–15) of the estrous cycle to evaluate LH secretory patterns. Indwelling jugular catheters were inserted on Day 7, and four cows had their catheters replaced on Day 14 prior to collection of the second serial blood sample because of loss of the catheter or coagulation of blood in the catheter during the period between collections. Samples were allowed to clot at room temperature, and then stored at 4°C until centrifugation. Serum was decanted and stored at -20°C until assayed for LH.

Radioimmunoassays

Concentrations of progesterone in plasma were quantified by RIA [22]. Intra- and interassay coefficients of variation for standard sera samples were 4.9% and 2.4%, respectively. Plasma concentrations of estradiol were quantified by RIA [23]. Intra- and interassay coefficients of variation for standard sera samples were 7.2% and 3.8%, respectively. Concentrations of LH in serum were analyzed by RIA using rabbit antiserum against ovine LH (TEA-RaOLH #35), highly purified ovine LH (LER-1374A) as radiolabeled tracer, and NIH-LH-B7 as standard [24]. Intra- and interassay coefficients of variation for standard sera samples were 10.7% and 8.7%, respectively.

Statistical Analysis

The experiment design was completely randomized. Data from one cow from each group were excluded from statistical analyses because of the development of two CL as a result of ovulation at estrus, as determined by ultrasonography. Means for CL area and progesterone concentrations were determined by repeated measures using the MIXED procedure of SAS [25]. Treatment, day, and treatment x day interaction were included in the model. Differences in least square means between the control group and treatment groups were determined using the PDIFF statement of SAS. Predetermined comparisons were made using single degree contrast statements. A contrast statement was included in the analysis for the control and the D3 group, and another contrast statement was used for the control and the D12 group. Preliminary analyses showed no difference between intact and unilaterally ovariectomized cows within a treatment group; therefore, data from intact and unilaterally ovariectomized females within a treatment group were analyzed together.

Mean and basal concentrations of LH (ng/ml) in serum, and frequency of LH pulses (pulses/16 h), and amplitude of LH pulses were analyzed by Pulsar (Pulsar software modified for IBM-PC by J.F. Gitzen and V.D. Ramirez, Urbana, IL). The pulses of LH secretion were determined with G values of 100, 2.60, 1.92, 1.46, and 1.13 for G(1)–G(5), respectively. The differences in LH secretion between groups were analyzed by ANOVA using the general linear models procedure of SAS [25].


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
CL Size and Function

Mean plasma progesterone concentrations were greater (P < 0.001) in the D3 agonist-treated cows (7.23 ± 0.72 ng/ml) than in control cows (3.42 ± 0.72 ng/ml; Fig. 1). Although there was no difference in the mean progesterone concentrations throughout the estrous cycle between the D12 group and the control cows, progesterone concentrations did increase (P < 0.05) on Day 16 and Day 17 for the D12 group compared with control cows. The luteal phase, as defined by number of days that progesterone concentrations were >1 ng/ml, was longer (P < 0.05) for the D3 group (17.42 ± 1.22 days) than for the control group (14.25 ± 0.70 days). The length of the luteal phase in the D12 group (15.92 ± 0.54 days) did not differ from that in the D3 or control groups.



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  		FIG. 1. Mean plasma progesterone concentrations from Day 3 to Day 18 of the estrous cycle for control cows (CONT, n = 6), D3 GnRH agonist-treated cows (D3, n = 6), and Day 12 GnRH agonist-treated cows (D12, n = 6). *Mean progesterone concentrations are significantly different (P < 0.001) for CONT and D3-treated cows

Area of the CL (cm2) that developed during the estrous cycle (Days 6–18) was larger (P < 0.001) for D3 cows (3.99 ± 0.25 cm2) than for control cows (2.78 ± 0.25 cm2; Fig. 2). There was no difference in area of the CL between D12 (3.03 ± 0.25 cm2) and control cows.



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  		FIG. 2. Area of the CL (cm2) in control cows (Cont; n = 6) and cows treated with GnRH agonist beginning on Day 3 (D3; n = 6) or Day 12 (D12; n = 6) of the estrous cycle. *CL area is significantly different (P < 0.001) for CONT and D3-treated cows

Concentrations and Secretion Pattern of LH and Progesterone

On Day 7, as expected, mean LH (ng/ml), basal LH (ng/ml), and LH pulse frequency (pulses/16 h) and amplitude (ng/ml) did not differ for D12 and control cows (Fig. 3 and Table 1). Mean and basal concentrations were enhanced (P < 0.01) on Day 7 for D3 compared with control cows. Pulsatile release of LH and pulse amplitude were unaffected by GnRH agonist administration.



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  		FIG. 3. Representative LH profiles for the Day 7 (A, C, and E) and Day 14 (B, D, and F) serial blood samples for control (A and B), Day 3 GnRH agonist-treated (D3; C and D), and Day 12 GnRH agonist-treated (D12; E and F) cows


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  		TABLE 1. Mean and basal LH concentrations, LH pulse frequency, and LH pulse amplitude in Day 7 serial blood samples from cows treated with GnRH agonist (azagly nafarelin) from Day 3 to Day 21 (D3) or Day 12 to 21 (D12) compared with control (CONT) cows

On Day 14, mean concentration of LH was greater (P < 0.01) in D12 than in control cows (Fig. 3 and Table 2). There tended to be a difference (0.05 < P < 0.10) on Day 14 in mean concentration of LH for D3 compared with control cows. Basal LH concentrations were greater (P < 0.05) on Day 14 for D3 than for control cows and greater (P < 0.001) for D12 than for control cows. Frequency of LH pulses was not different (P > 0.10) on Day 14 among groups. Amplitude of LH pulses was less (P < 0.01) on Day 14 for D3 and D12 cows than for control cows.


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  		TABLE 2. Mean and basal LH concentrations, LH pulse frequency, and LH pulse amplitude in Day 14 serial blood samples from cows treated with GnRH agonist (azagly nafarelin) from Day 3 to Day 21 (D3) or Day 12 to 21 (D12) compared with control (CONT) cows

Pattern of Estrous Behavior and Ovulation after Cessation of GnRH Agonist Treatment

Administration of the GnRH agonist beginning on Day 3 increased the interestrus interval (25.82 ± 3.60 days), but this increase was not significantly different when compared with the D12 or control groups (21.50 ± 1.05 days and 21.00 ± 1.26 days, respectively). However, only one cow in the D3 group ovulated at a time associated with the first behavioral estrus after discontinuing GnRH agonist treatment. The remainder of the cows in the D3 group expressed behavioral estrus as detected by being mounted by other cows, but ovulation with an associated behavioral estrus was not detected until Days 28, 30, 32, and 43 relative to the original day of estrus (Day 0 in study) as determined by ultrasonography. Similar patterns for expression of behavioral estrus that was not associated with ovulation occurred in cows of the D12 group, with behavioral estrus occurring several days before the time when the first ovulation associated with a behavioral estrus was detected on Days 30, 32, 38, 40, and 46. One cow each from the D3 and D12 groups did not ovulate by Day 84 when evaluation for ovulation by ultrasonography was discontinued. Ovulation data were not recorded for control cows, but it was assumed ovulation occurred approximately 30 h after onset of estrus, as is typical for cattle (21.00 ± 1.26 days). The actual time of ovulation was not evaluated in the present study.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
GnRH Effects on Luteal Function in Cattle

In support of our working hypothesis, luteal function was enhanced when GnRH agonist was administered chronically beginning in the early luteal phase (Day 3). However, GnRH agonist treatment beginning in the midluteal phase (Day 12) also enhanced luteal function on Days 16 and 17. Previous findings [20] indicate that the CL is not dependent on pulses of LH from Day 12 to Day 17 (Day 0 = estrus). In that previous study, luteal function in cows was unaffected by administration of an antagonist of GnRH from Day 12 to Day 17 of the estrous cycle. In the present study, however, luteal function was enhanced by GnRH agonist administration from Day 12 to Day 21; therefore, the fully functional CL might be responsive to alterations of LH secretion that are nonpulsatile in manner.

Luteotropin Actions on Luteal Function in Cattle

Administration of hCG [26] or GnRH agonist [15] induced ovulation of the dominant follicle and consequently formation of an accessory CL in cows. Schmitt et al. [15] reported increased progesterone concentrations from Day 6 to Day 13 when GnRH agonist or hCG was administered on Day 5. However, it was unknown if the increased concentrations of progesterone resulted from stimulation of the original CL or the induction of an accessory CL.

Based on a previous study from our laboratory (unpublished results), luteal function is not altered by destruction of ovarian follicles via aspiration during the estrous cycle. Enhanced luteal function in the present study cannot, therefore, be explained by use of the experimental technique of follicular aspiration. In the present study, induced CL or luteinized follicles were not formed because follicles >4 mm in diameter that may have been responsive to the acute elevation of LH after the administration of GnRH were destroyed by follicular aspiration before GnRH agonist administration. The presence of a single CL and absence of follicular luteinization was confirmed by daily ultrasonography. The enhanced plasma progesterone concentrations in the present study were, therefore, due to the enhanced function of the original CL and not to an induced CL resulting from the ovulation of another follicle at the time of GnRH administration. This finding is supported by the increased CL size in the GnRH agonist-treated groups.

Concentrations of LH and Progesterone as Controlled by Exogenous GnRH in Cattle

There is an acute elevation of LH after administration of GnRH agonist, and this elevation of LH release continues for approximately 24 h before returning to basal concentrations [7, 19]. The acute increase in plasma concentrations of LH when cows are implanted with GnRH agonist for relatively short periods (as compared with the present study and the other treatment group in the previous study) from Day 2 to Day 5 does not enhance luteal function (unpublished results). In addition, treatment with 100 µg GnRH on Day 2 of the estrous cycle reduces serum progesterone concentrations during the following midluteal phase of the estrous cycle [27]. Therefore, although LH is a luteotropin, additional LH stimulation of the CL during the early luteal phase without subsequent exogenous GnRH treatment to enhance LH secretion may compromise subsequent luteal function [27]. Martin et al. [13] suggested that impairment of luteal function is due to desensitization of the CL to further stimulation by LH.

Chronic administration of GnRH agonist and the resulting increased basal LH concentration enhanced luteal function in the present study. In a previous study, we speculated that enhanced progesterone secretion is the result of increased basal LH secretion in cows treated for longer periods with GnRH agonist, but serial blood samples were not collected to test this hypothesis (unpublished results). In the present study, serial blood sampling revealed that induced basal LH concentrations were enhanced throughout the period of GnRH agonist treatment.

Existing evidence indicates that enhanced progesterone secretion from the CL of cows treated with GnRH agonist is not caused by direct action of GnRH at the CL but rather by the altered secretion of LH resulting from GnRH administration. Receptors for GnRH have not been identified in the ovaries [28] or luteal cells [29] of cattle. Until recently, evidence indicated that there was no mRNA for GnRH receptors in the CL of cattle [30], but preliminary information now indicates that GnRH receptor mRNA is present in CL and follicles of cattle ovaries [31]. However, there is still no evidence of functional GnRH receptors in the CL of cattle. The present findings therefore suggest that the impact of GnRH on luteal size and function is not due to direct actions of GnRH at the CL.

Potential Actions of GnRH on Luteal Function

As the CL develops, small luteal cells differentiate into large luteal cells [32]. Administration of GnRH agonist on Day 0 [11] or on Day 7 [33] increased the ratio of large luteal cells to small luteal cells. When ewes were treated with LH, small luteal cells were converted to large luteal cells in the midluteal phase CL [34]. With nearly 80% of secreted progesterone being synthesized by the large luteal cells [35], we speculated that administration of GnRH agonist indirectly increases the number of large luteal cells and, therefore, secretion of progesterone by the CL is enhanced.

Behavioral Estrus and Ovulation after Cessation of Chronic Treatments with GnRH Agonist

Although the objective of the present study focused on CL function in cows treated with GnRH agonist, there were significant post hoc observations that were of physiological significance. Four cows in the D3 group still had a functional CL at the time of cessation of treatment. Hence, progesterone inhibited final maturation of the dominant follicle and behavioral estrus in these four cows at the time of cessation of GnRH agonist treatment. After luteal regression subsequent to cessation of GnRH agonist treatment, all four of these cows displayed behavioral estrus and ovulated from the first dominant follicle that developed subsequent to cessation of GnRH agonist treatment. In those cows in which the CL had regressed at the time of treatment cessation, behavioral estrus was observed in 8 of 12 GnRH agonist-treated cows within a few days after cessation of GnRH agonist treatment, but there was no ovulation associated with this estrus in 7 of these cows. The one cow (D3 group) that returned to estrus and ovulated subsequent to this estrus had increased basal LH concentrations during treatment with GnRH agonist but did not have increased plasma progesterone concentrations during the luteal phase to the extent that occurred in the other D3 cows. For the remaining seven GnRH agonist-treated cows, the initial preovulatory sized follicle that developed subsequent to cessation of GnRH agonist treatment became atretic and a new dominant follicle appeared. Ovulation occurred from the subsequent preovulatory large follicle that developed in all but three of these cows. One cow ovulated the third preovulatory dominant follicle that developed, and the remaining two cows, one from each treatment group (D3 and D12), developed persistent follicles, and ovulation had not occurred by Day 84, when ultrasonographic evaluation of ovaries was stopped. Dominant follicle growth was not attenuated with chronic GnRH agonist treatment in the present study, as has been reported by others [36–38]. In the previous studies, the objective was to determine whether chronic administration of a GnRH agonist alters ovarian follicular dynamics. However, in the present study observations of follicular dynamics were post hoc and as part of the experimental design follicles responsive to LH were aspirated prior to administration of the agonist, altering the emergence of new follicles. Therefore, no direct comparison of ovarian follicular dynamics under conditions of chronic GnRH agonist treatment can be made between the present and previous studies.

Some GnRH agonist-treated cows exhibited behavioral estrus but did not ovulate in conjunction during the initial estrous cycle after cessation of GnRH agonist treatment [39]. The large follicles may have been responsive to LH, and there might have been enough LH secreted to stimulate synthesis of adequate amounts of estradiol to induce behavioral estrus after cessation of GnRH agonist treatment. The pituitary, however, may have remained desensitized to GnRH to the extent that there was no preovulatory surge of LH and no ovulation associated with estrus in some cows [39]. Bergfeld et al. [18] reported that pituitaries of bulls remained desensitized for at least 20 days after 28 days of treatment with the GnRH agonist deslorelin. Pituitary desensitization also occurs in heifers after cessation of treatment with a GnRH agonist [19]. Pituitary desensitization may be in part due to downregulation of GnRH receptors at the pituitary [7].

Conclusions

Chronic administration of GnRH agonist from Day 3 to Day 21 and from Day 12 to Day 21 of the estrous cycle enhanced luteal function and increased CL size in the GnRH agonist-treated cows compared with control cows. Although the LH pulse was not totally suppressed as expected based on previous research [20], the significant increase of basal LH concentrations as a result of GnRH agonist treatment probably induced the enhanced luteal function observed in the D3 and D12 GnRH agonist-treated cows compared with control cows. Long-term administration of the GnRH agonist resulted in a delay of the subsequent ovulation in some of the GnRH agonist-treated cows, probably as a result of partial pituitary desensitization. Therefore, although chronic administration of GnRH agonist to cows enhanced luteal function, the pituitary desensitization that occurred in individual animals is still of concern if such treatments are to be used in the cattle industry to enhance luteal function and pregnancy rates. Nonetheless, the present results indicate that luteal function is enhanced when GnRH agonist is administered during either the early or midluteal phase, probably as a result of the increased basal LH concentrations in blood plasma that stimulate the CL. We reject our working hypothesis that luteal function and CL size are enhanced in cattle administered an agonist of GnRH only when the CL is in the developmental stages, because CL function was also enhanced when administration of agonist was initiated after the CL was fully functional.


   ACKNOWLEDGMENTS
 
We thank Candy Toombs for her technical assistance with the RIA and Jeanne Osborne for assistance in editing the manuscript. This article is published as Paper 13674 in the Journal Series of the Nebraska Agricultural Research Division and as Paper 44-02AS of the Ohio Agricultural Research and Development Center.


   FOOTNOTES
 
1 This research was supported by USDA Animal Health Formula Funding to the University of Nebraska. Back

2 Correspondence: James E. Kinder, 110B Animal Science, 2029 Fyffe Rd., Ohio State University, Columbus, OH 43210-1095. FAX: 614 292 2929; kinder.15{at}osu.edu Back

3 Current address: Department of Animal Sciences, 207 Gerlaugh Hall, 1680 Madison Ave., OARDC, Wooster, OH 44691-4096 Back

4 Current address: Department of Animal Sciences, Ohio State University, 3638 Kays Ave., Dublin, OH 43017. Back

5 Current address: CENID Fisiologia y Mejoramiento Animal, INIFAP-SAGARPA, Apdo. Postal 2-29, Queretaro, Queretaro, Mexico Back

Received: 27 November 2002.

First decision: 17 December 2002.

Accepted: 12 March 2003.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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