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BOR - Papers in Press, published online ahead of print February 5, 2003.
Biol Reprod 2003, 10.1095/biolreprod.102.013532
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BIOLOGY OF REPRODUCTION 69, 141–145 (2003)
DOI: 10.1095/biolreprod.102.013532
© 2003 by the Society for the Study of Reproduction, Inc.

Neuroendocrinology

Different Effects of Subnormal Levels of Progesterone on the Pulsatile and Surge Mode Secretion of Luteinizing Hormone in Ovariectomized Goats1

Seungjoon Kim, Tomomi Tanaka, and Hideo Kamomae2

Laboratory of Veterinary Reproduction, Tokyo University of Agriculture and Technology, Fuchu, Tokyo 183-8509, Japan


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
This study tested the hypothesis that endocrinological threshold levels of progesterone that induce negative feedback effects on the pulsatile and surge modes of LH secretion are different. Our approach was to examine the effects of subnormal progesterone concentrations on LH secretion. Long-term ovariectomized Shiba goats that had received implants of silastic capsules containing estradiol were divided into three groups. The high progesterone (high P) group received a subcutaneous implant of a silastic packet (50 x 70 mm) containing progesterone, and the low progesterone (low P) group received a similar implant of a small packet (25 x 40 mm) containing progesterone. The control (non-P) group received no treatment with exogenous progesterone. Blood samples were collected daily throughout the experiment for the analysis of gonadal steroid hormone levels and at 10-min intervals for 8 h on Days 0, 3, and 7 (Day 0: just before progesterone treatment) for analysis of the pulsatile frequency of LH secretion. Then estradiol was infused into the jugular vein of all animals at a rate of 3 µg/h for 16 h on Day 8 to determine whether an LH surge was induced. Blood samples were collected every 2 h from 4 h before the start of the estradiol infusion until 48 h after the start of the infusion. In each group, the mean ± SEM concentration after progesterone implant treatment was 3.3 ± 0.1 ng/ml for the high P group, 1.1 ± 0.1 ng/ml for the low P group, and <0.1 ng/ml for the non-P group, concentrations similar to the luteal levels, subluteal levels, and follicular phase levels of the normal estrous cycle, respectively. The estradiol concentration ranged from 4 to 8 pg/ml after estradiol capsule implants in all groups. The LH pulse frequency was significantly (P < 0.05) suppressed on Day 3 (6.2 ± 0.5 pulses/8 h) and on Day 7 (2.6 ± 0.9 pulses/8 h) relative to Day 0 (9.0 ± 0.5 pulses/8 h) in the high P group. In both the low P and non-P groups, however, the changes of pulsatile frequency of LH were not significantly different, and high pulses (7–9 pulses/8 h) were maintained on each of the 3 days they were tested. An LH surge (peak concentration, 100.3 ± 11.0 ng/ml) occurred in all goats in the non-P group, whereas there was no surge mode secretion of LH in either the high P or the low P group. The results of this study support our hypothesis that the threshold levels of progesterone that regulate negative feedback action on the LH pulse and the LH surge are different. Low levels of progesterone, around 1 ng/ml, completely suppressed the LH surge but did not affect the pulsatile frequency of LH secretion.

luteinizing hormone, ovary, progesterone


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The secretion of progesterone from the corpus luteum is controlled by hormonal signals from various organs, and LH from the anterior pituitary gland has been shown to be a key determinant of progesterone secretion that acts by modulating luteotropic and luteolytic functions in cows [1, 2], sheep [3], and monkeys [4]. Changes in the circulating progesterone level, in turn, influence the pulsatile and surge modes of LH secretion regulated by hypothalamic GnRH secretion through a negative feedback mechanism. Previous studies have indicated that the level of progesterone of the midluteal phase decreases the frequency of LH pulses [5] and GnRH pulses [6] and the level of hypothalamic electrical activity associated with GnRH pulse generation [7]. On the other hand, Kasa-Vubu et al. [8] demonstrated that the midluteal level of progesterone completely blocks the LH surge in ovariectomized ewes given estradiol by acting centrally to inhibit the surge of GnRH secreted into the hypophyseal portal system. Therefore, there is general agreement that midluteal levels of progesterone suppress the pulsatile and surge modes of LH secretion by influencing the hypothalamic GnRH neurosecretory system.

Subnormal levels of progesterone secretion are caused by abnormal conditions in domestic animals, e.g., in the cow with cystic corpus luteum [9] and in ewes exposed to stress [10]. However, the effects of subnormal levels of progesterone on the endocrine system remain unknown. In cycling cows, some reports have indicated that treatment with subnormal or low levels of progesterone induced by controlled intravaginal drug release resulted in continuous growth of the dominant follicle [11, 12] accompanied by a high frequency of LH pulses. The authors suggested that those findings were due to the lack of negative feedback action of progesterone on pulsatile LH secretion. On the other hand, the estradiol-induced LH surge is suppressed by low plasma concentrations of progesterone in dairy cows [13]. Those studies indicated the possibility that a subnormal level of progesterone has differential negative feedback effects on the pulsatile and surge modes of secretion of LH.

The objective of the present study was to test the hypothesis that endocrinological threshold levels of progesterone that induce negative feedback effects on the pulsatile and surge modes of LH secretion are different. The Shiba goat has been proven to be a useful experimental animal for scientific studies of domestic ruminants, and neurophysiological [14], endocrinological [15], and clinical [16] approaches have been established for studying reproductive function. Our approach in the present study was to determine whether treatment with a low level of progesterone equivalent to the level in the subluteal phase influenced simultaneously the frequency of the LH pulse and the estradiol-induced LH surge in ovariectomized Shiba goats.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Animals

Nine long-term ovariectomized Shiba goats weighing between 20 and 30 kg (mean ± SD, 24.6 ± 1.9 kg) were used. Shiba goats are nonseasonal breeders under natural daylight [17]. The goats were ovariectomized at least 3 mo before the start of the experiment and were maintained outdoors with a diet of hay-cubes given twice daily and water given ad libitum. Basically, the animals in this study were divided into three groups in a 3 x 3 Latin square design (finally, n = 4 or 5 for each group), and at least 4 wk were allowed to elapse after each treatment. All animals were housed and loose-tied at the start of the experiment.

Implantation and Infusion of Ovarian Steroids

All animals initially received implants of silastic capsules (inside diameter, 3.35 mm; outside diameter, 4.65 mm; length, 40 mm; Dow Corning Co., Midland, MI) containing crystalline estradiol (Sigma, St. Louis, MO) subcutaneously as reported previously [18, 19], which induced levels similar to luteal levels of estradiol (3–10 pg/ml) [17, 18]. Seven days later, they were separated into three groups according to the use of an exogenous device for providing progesterone: a high progesterone (high P) group that received a subcutaneous implant of a silastic packet (50 x 70 mm; Dow Corning) containing crystalline progesterone (Wako, Tokyo, Japan), which reproduces the plasma progesterone level in the midluteal phase (3–8 ng/ml) [7, 18], and a low progesterone (low P) group that received a subcutaneous implant of a smaller packet (25 x 40 mm; Dow Corning) containing crystalline progesterone, which imitated subluteal levels of progesterone (around 1 ng/ml). The control (non-P) group had no implant progesterone treatment, which paralleled to follicular levels of progesterone (<0.1 ng/ml) [16, 17]. Daily blood sampling (5 ml) was conducted throughout the experiment to monitor the steroidal level in the circulation. Blood samples were collected every 10 min for 8 h just before progesterone treatment (Day 0) and 3 days (Day 3) and 7 days (Day 7) after progesterone treatment for analysis of LH pulses. Then all animals were given estradiol on the day after last repetitive sampling (Day 8) for analysis of the effect on the LH surge. Estradiol (Sigma) was dissolved in ethanol (100 µg/ml), diluted with sterilized saline to a concentration of 0.3 µg/ml, and infused with a peristaltic mini pump (SJ-1211; Atto, Tokyo, Japan) into the jugular vein at a rate of 3 µg/h for 16 h through one of the catheters fitted bilaterally to the jugular vein, as previously described [20]. This treatment is known to be able to induce an LH surge starting approximately 10 h after the start of estradiol infusion in ovariectomized goats, as described previously [20]. Blood samples (2 ml) were collected via another jugular catheter at 2-h intervals for 52 h (from 4 h before the start of estradiol infusion to 48 h after the start of estradiol infusion) for analysis of the plasma concentrations of LH and estradiol.

Blood Sampling

Blood samples for analysis of the LH pulse and LH surge were collected from the catheterized jugular vein into heparinized tubes. A catheter (18 gauge, 51-mm length; Terumo Co., Tokyo, Japan) was inserted into the jugular vein just before the start of blood sampling. Blood samples were immediately stored at 4°C and centrifuged at x3000 rpm for 20 min, and then plasma was stored at -20°C until assayed for LH, progesterone, and estradiol.

Hormone Assays

Plasma concentrations of progesterone and estradiol were assayed by a previously described method [21]. The sensitivity of the assays for progesterone and estradiol were 0.015 ng/ml and 0.69 pg/ml, respectively. The intra-assay and interassay coefficients of variation were 8.22% and 0.2% for progesterone and 7.37% and 0.19% for estradiol, respectively.

Plasma concentrations of LH were measured by a double-antibody radioimmunoassay [15]. The following reagents were used: NIADDK-ovine LH-1–3 for radioiodination, NIADDK-ovine LH-25 as a standard, anti-ovine LH rabbit serum (YM No. 18) as the first antibody, and goat anti-rabbit immunoglobulin as the second antibody. The sensitivity of the assay was 0.1 ng/ml. The intra-assay and interassay coefficients of variation were 6.77% and 0.12%, respectively.

Statistics

Data were analyzed using the Scheffe method of analysis of variance with the StatView computer program (StatView 4.5; Abacus Concepts Inc., Berkeley, CA). During the implantation of steroids, one-way analysis of variance was also used to determine the significance of differences among the mean concentrations of progesterone and estradiol among the three groups. All data are presented as mean ± SEM. The LH pulse was identified using the Cluster Analysis Program [22]. The LH surge was defined as the point when a sustained rise (for at least two consecutive points of blood sampling) in the plasma LH concentration exceeded twice the average baseline level during the pretreatment period before the estradiol infusion.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Plasma Concentrations of Progesterone and Estradiol

The concentration of estradiol was increased the day after the implantation of estradiol capsules and was maintained at a basal level (4–8 pg/ml) up to Day 7 in all animals (Fig. 1). The plasma progesterone concentrations were increased after the treatment with progesterone in the high P and low P groups but not in the non-P group (Fig. 1). The mean concentration of progesterone was maintained at the levels of the midluteal phase (range, 2.09–5.49 ng/ml; mean ± SEM, 3.3 ± 0.1 ng/ml) and the subluteal level (range, 0.61–2.59 ng/ml; mean ± SEM, 1.1 ± 0.1 ng/ml) in the high P and low P groups, respectively. There were significant differences among the three groups in the mean plasma concentrations of progesterone on all the days examined after the progesterone treatment (P < 0.05).



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  		FIG. 1. Plasma progesterone (top, mean ± SEM) and estradiol (bottom) concentration during the period of progesterone/estradiol implantation (black rectangle, progesterone implant; blank rectangle, estradiol implant). Changes in plasma estradiol concentration during estradiol infusion on Day 8 (shaded rectangle, estradiol infusion; inset in bottom figure). High P, High progesterone group, treated with a large packet (50 x 70 mm); low P, low progesterone group, treated with a small packet (25 x 40 mm); non-P, no implant treatment

Patterns of Pulsatile LH Secretion

Representative patterns of pulsatile LH secretion before and after progesterone treatment in the three groups are shown in Figure 2, and the number of LH pulses on Day 0, Day 3, and Day 7 is summarized in Table 1. There was no significant difference in the frequency of LH pulses among the three groups on Day 0 (P > 0.1). The frequency of LH pulses in the high P group was significantly decreased gradually after the progesterone treatment (P < 0.05), whereas there was no significant reduction of LH pulse frequency in the low P and non-P groups (P > 0.1). On Day 3 and Day 7, the frequencies of the LH pulses in the high P group were significantly lower than those in the low P and non-P groups (P < 0.05), and there was no significant difference in the frequency of LH pulses between the low P and non-P groups (P > 0.1).



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  		FIG. 2. Patterns of pulsatile luteinizing hormone (LH) secretion in representative animals from the high progesterone (high P) group (right panels), low progesterone (low P) group (middle panels), and control (non-P) group (left panels) on the day just before the progesterone treatment (Day 0, upper) and on the third day (Day 3, middle) and seventh day (Day 7, bottom) of progesterone treatment. Arrowheads indicate the LH pulses identified by using the Cluster Analysis Program


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  		TABLE 1. The pulsatile frequency of luteinizing hormone (pulses/8 h) after treatment with luteal (high P) and subnormal (low P) levels of progesterone in ovariectomized goats given a basal level of estradiol.a

Occurrence of LH Surges

The plasma concentrations of estradiol ranged from 30.2 to 105.2 pg/ml during estradiol infusion in the three groups, and there was no significant difference in the estradiol concentration among these three groups (Fig. 1). The changes in the LH concentration after estradiol infusion in all the animals examined are shown in Figure 3. An LH surge was induced in all four cases of the non-P group. The mean level of the peak of the LH surge reached 100.3 ± 11.0 ng/ml, and the time interval from estradiol infusion until the peak of LH surge was 11.5 ± 1.0 h. In the high P and low P groups, the plasma concentrations of LH remained low until 48 h after the start of estradiol infusion, and no occurrence of LH surge was found in any of the animals.



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  		FIG. 3. Profiles of luteinizing hormone (LH) concentration after the start of estradiol infusion in the high progesterone (high P, upper), low progesterone (low P, middle), and control (non-P, bottom) groups. Estradiol was infused at the rate of 3 µg/h through the jugular vein for 16 h, as indicated by the shaded rectangle. Each panel shows the LH patterns of all animals in the respective group


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The present results agree with previous reports showing that plasma progesterone concentrations were increased and then maintained at the expected concentration when devices designed to provide exogenous treatments, such as subcutaneous or intravaginal application, were used [1, 6, 8, 11]. Some reports have suggested that the plasma concentration of progesterone is influenced by environmental factors [23, 24] and nutritional conditions [25, 26] in ruminant animals. However, in the present study, the plasma concentrations of progesterone in the low P group were maintained at around 1 ng/ml, and this is similar to the level observed in abnormal conditions, such as ovarian disorders [9], stress [10], and luteal hypoplasia of Shiba goats [unpublished results]. Thus, the subluteal level of the progesterone concentration was probably mimicked throughout the experiment in the present study. Low concentrations of progesterone had no effect on the LH pulses, whereas they inhibited the estradiol-induced LH surge. It is unlikely that this discrepancy was due to an insufficient dose of estradiol-17ß infusion, since the concentration of estradiol ranged from 54.7 to 89.0 pg/ml, which slightly exceeded the peak level of plasma estradiol in the estrous phase of Shiba goats [7]. Nanda et al. [13] have clearly shown that progesterone concentrations of more than 0.7 ng/ml in plasma induced by progesterone-releasing intravaginal device (PRID) insertion inhibited the estradiol-induced LH surge in intact and ovariectomized cows. The present study supported the previous observation that such low levels of progesterone were able to block the estradiol-induced LH surge.

On the other hand, the present results clearly indicated that subluteal levels of progesterone that completely inhibit the LH surge are not able to suppress the pulsatile secretion of LH. This finding suggests that the negative feedback actions of progesterone on the pulsatile and surge modes of secretion of LH are influenced independently by different threshold levels of progesterone. This idea is consistent with previously reported observations that anovulatory persistent follicular development is associated with low levels of progesterone produced by PRID treatment [11, 12] or caused by ACTH treatments or stress [10, 27]. In those cases, it is likely that follicular growth is stimulated by the high frequency of LH pulses, but ovulation is blocked by the lack of an LH surge under subluteal conditions. The mechanism of the different actions of subnormal progesterone levels on the pulse and surge modes of the secretion of LH could be explained by the theory of the neural mechanism of hypothalamic GnRH secretion. Recently, several reports have suggested that there are two independent neural generators of GnRH neurosecretion, i.e., a GnRH pulse generator that regulates the LH pulse and a GnRH surge generator that regulates the LH surge [7, 20, 28, 29]. According to this theory, it seems that the luteal levels of progesterone suppress both generators, but subnormal levels of progesterone affect only the GnRH surge generator, suggesting that the GnRH surge generator is more sensitive to the negative feedback caused by progesterone than the pulse generator.

It is difficult to precisely determine the threshold levels of progesterone required to affect the pulse and surge modes of secretion of LH. However, the present study suggested that the threshold levels of progesterone for the suppression of LH secretion appear to be more than around 2.5 ng/ml for the pulse and less than 1 ng/ml for the surge modes. The reciprocal relationship between the LH pulse frequency (or GnRH pulse generator activity) and plasma progesterone level has been clearly demonstrated during the estrous cycle in ruminant species, including the goat [7]. Sanchez et al. [30] reported that the frequency of pulsatile LH secretion was related to the dose of synthetic progestin in heifers. Consequently, the LH pulse frequency is not suppressed by low levels of progesterone (1–2.5 ng/ml in the present study), whereas the suppressive effect of progesterone on the LH pulse frequency seems to occur in a dose-dependent manner in response to changes in the circulating progesterone when the progesterone concentration is above a threshold level (>2.5 ng/ml in the present study).

The frequency of the LH pulse was suppressed in the group with high levels of progesterone in a time-dependent manner, and the pulsatile frequency of LH was significantly less on Day 7 than on Day 3. The present findings are consistent with previous reports showing that gonadotropin secretion was not inhibited immediately by the synergistic effects of progesterone and estradiol in ovariectomized [31] and intact [1] cows. However, they do not agree with findings that the LH pulse frequency was decreased within 6 h after changing the circulating concentration of progesterone and that this suppressive effect became constant within 24 h [32]. In the previous study [32], intact bovine females were used, whereas we used long-term (>3 mo) ovariectomized goats. The reason for the disagreement between these previously reported and the present results may be related to differences of either the species or the endogenous steroidal milieu before the start of the experiment.

The results of this study have clearly demonstrated that subluteal levels of progesterone around 1 ng/ml completely suppressed the LH surge but had no inhibitory effect on the pulsatile frequency of LH secretion. The present results support the hypothesis of Stock and Fortune [11] that a high frequency of LH pulses maintains the growth of dominant follicles and increases estradiol production, leading to cystic follicles and anovulation. Therefore, further studies may be necessary to explore the progesterone negative feedback mechanism regulating the pulsatile and surge modes of secretion of LH and the hypothalamic GnRH regulatory system to fully clarify the mechanism of hormonal control of ovarian function.


   ACKNOWLEDGMENTS
 
We thank Dr. Gordon D. Niswender, Colorado State University, for providing reagents used in the progesterone and estradiol radioimmunoassay, and Drs. Yuji Mori, University of Tokyo, and Gen Watanabe, Laboratory of Veterinary Physiology of our university, for providing reagents used in the LH radioimmunoassay.


   FOOTNOTES
 
1 This study was supported in part by a grant-in-aid for scientific research from Tokyo University of Agriculture and Technology. Back

2 Correspondence: Hideo Kamomae, Laboratory of Veterinary Reproduction, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai, Fuchu, Tokyo 183-8509, Japan. FAX: 81 42 366 4062; kamomae{at}cc.tuat.ac.jp Back

Received: 15 November 2002.

First decision: 2 December 2002.

Accepted: 4 February 2003.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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