Lactational [correction of Lacational] anovulation in rats and its dependency on progesterone

The relationship between prolactin (PRL) secretion and anovulation in lactating rats was studied. Normal lactating rats and lactating rats treated with antiserum against luteinizing hormone-releasing hormone at the time of postpartal ovulation were used. Normal lactating rats were treated with either a dopamine agonist (CB-154, 150 micrograms/rat) on Day 10 or 13, or pups removal on Day 7 or 10, and thereafter luteolysis and inhibition on PRL secretion were assessed. With the CB-154 treatment, the incidence of luteolysis increased as the lactational period advanced (42% vs 72%), whereas it decreased (73% vs 14%) with the pups removal. Thus, dopamine effectively inhibited PRL secretion during the later lactational stage, but could not do so during the earlier stage when there were mechanisms other than dopamine stimulating PRL secretion. Following luteal regression induced by CB-154, ovulation did not occur if the rats were treated with CB-154 on Day 10, whereas 50% of the rats ovulated within 4 days if treated on Day 13. Furthermore, in the lactating rats treated with anti-luteinizing hormone-releasing hormone serum during late pregnancy, ovulation was not observed until Day 10 of lactation. Since the serum progesterone levels were low in these rats due to the absence of ovulation and lactational corpora lutea, the blockade of ovulation was not due to elevated circulating progesterone during the early lactational period. The mechanism of ovulation blockade during lactation thus seems to shift from being progesterone independent to progesterone dependent at a similar period when the neuroendocrine control of PRL secretion shifts from dopamine independent to dependent.     

The ovary of the wood mouse, Apodemus sylvaticus, during late pregnancy and lactation

Female wood mice, Apodemus sylvaticus, were killed on day 18 of pregnancy (P 18) and on days 0, 3, 6, 9, 12, 15, and 18 of lactation (L 0, L 3, L 6, L 9, L 12, L 15, and L 18 respectively), and the ovaries were studied. The weight of the ovaries was recorded at dissection. The corpora lutea and the follicles of the right ovary were counted and measured, and the appearance of the interstitial tissue was noted. A decline in weight from day P 18 to day L 6 coincided with a decrease in mean diameter of the corpora lutea. The mean number of corpora lutea did, however, not change over the period. The corpora lutea present throughout lactation were probably from the gestation period; the females did not appear to ovulate post-partum. The interstitial tissue was not affected, as far as could be judged with light microscopy. Ovulatory follicles were only present at times close to expected ovulation; on days P 18 and L 18. A lactational anoestrous is suggested for the wood mouse.     

Effect of prostaglandin F2 alpha on release of progesterone and leukotriene B-4 by cells from corpora lutea of mares.

Corpora lutea were recovered from mares either 4 to 5 days or 12 to 13 days after ovulation. Mixed populations of luteal cells were prepared by collagenase digestion and were incubated for 24 h in the presence or absence of prostaglandin (PG) F-2 alpha (250 ng/ml). PGF-2 alpha significantly (P = 0.03) reduced progesterone secretion by cells from late diestrous corpora lutea and tended (P = 0.06) to reduce secretion by early diestrous cells. PGF-2 alpha had no significant effect on leukotriene B-4 (LTB-4) production by cells from early diestrous corpora lutea, but significantly (P = 0.03) increased LTB-4 production by late diestrous luteal cells. It seems possible that LTB-4 could play a role as an intermediary in the action of PGF-2 alpha in luteolysis in the mare.     

Effect of prostaglandin E2 alpha on the hCG-stimulated progesterone production by human corpora lutea

The effect of prostaglandin PGF2 alpha on the hCG stimulated and basal progesterone production by human corpora lutea was examined in vitro. hCG (40 i.u./ml) stimulated progesterone formation in corpora lutea of early (days 16-19 of a normal 28 day cycle), mid (days 20-22) and late (days 23-27) luteal phases. This stimulation was inhibited by PGF2 alpha (10 micrograms/ml) in corpora lutea of mid and late luteal phases. PGF2 alpha alone did not show a consistent effect on basal progesterone production. The inhibition of hCG stimulated progesterone production by PGF2 alpha at times corresponding to luteolysis indicates a role for that prostaglandin in the process of luteolysis in the human corpus luteum.     

Pregnancy, lactation and the oestrous cycle of the pouched mouse, Saccostomus campestris

The anatomy and histology of pouched mouse ovaries were studied during the oestrous cycle, pregnancy and lactation along with the relationship between the ovarian structures and circulating concentrations of progesterone. The structure of the ovaries resembled that of most rodents. Follicular development indicated that ovulation takes place on the night between pro-oestrus and oestrus, i.e. at the time when mating normally occurs. Corpora lutea were accumulating in cyclic females, while successively disappearing during pregnancy, leaving only the set formed after conception. After parturition luteal regression was rapid. Theca interna, included in the corpora lutea, formed glandular stromal tissue after regression of the luteal tissue formed from granulosa cells. The progesterone profile of non-pregnant females indicated a short but functional luteal phase (peak at metoestrus) during the cycle. During pregnancy three peaks of progesterone stood out: (1) when implantation starts, (2) when older sets of corpora lutea showed rejuvenation and placental signs were found in the vaginal smears, and (3) 3 days before expected parturition when luteal development (as judged by histology) reached a peak. The placenta may participate in but not 'take over' the progesterone production during later stages of pregnancy. Very low concentrations of peripheral progesterone during lactation and a very low level of follicular development at that time support an earlier suggestion of a lactational anoestrus in pouched mice.     

Changes in plasma progesterone and prolactin concentrations during the annual cycle and the role of prolactin in the maintenance of lactation and luteal development in the Antarctic fur seal (Arctocephalus gazella)

Progesterone in Antarctic fur seals was undetectable from 1-2 days before parturition to 4-6 days after parturition. There was a rapid increase in progesterone to 20 ng/ml between 6 and 10 days post partum and this increase coincided with peak concentrations of oestradiol-17 beta at the time normally associated with oestrus and mating in this species. Newly formed corpora lutea were present in the ovaries by Day 9 post partum even though the seals had been isolated in an enclosure and not mated. Thereafter, progesterone remained detectable, but at a low concentration (5 ng/ml) throughout embryonic diapause. A similar pattern was observed in unmated females which suggests they enter a period of pseudopregnancy. Progesterone increased to 35 ng/ml between late February and mid-March, indicating activation of the corpus luteum at the end of diapause, and then declined slowly through the remainder of gestation. Plasma prolactin, measured against a human prolactin standard, was elevated from 1-2 days before parturition and peaked at 0-3 days post partum. It then declined slowly throughout the post-partum period and remained at a low level throughout embryonic diapause. Prolactin concentration declined to undetectable at the end of diapause and before the end of lactation. Reduction of prolactin secretion by injections of bromocriptine from Days 3 to 5 post-partum terminated lactation. Mothers, which normally leave their pups to feed at sea on about Day 7 post partum, did not continue to lactate beyond Day 7 although this did not appear to be associated with reduced prolactin secretion. Bromocriptine treatment appeared to prevent the post-ovulatory surge of progesterone although there was no long-term effect of bromocriptine on progesterone secretion during the early stages of embryonic diapause/pseudopregnancy. This study has shown that prolactin is an important hormone for maintaining early lactation in the fur seal and it probably also has a role in the control of ovulation and luteal development. Prolactin does not appear to be implicated in the control of lactation cycles in fur seals. Changes in plasma progesterone during the annual cycle show that the pattern in fur seals resembles that of some carnivores with embryonic diapause.     

Effect of prostaglandin F2α on the hCG-stimulated progesterone production by human corpora lutea

The effect of prostaglandin PGF_2α on the hCG stimulated and basal progesterone production by human corpora lutea was examined . hCG (40 i.u./ml) stimulated progesterone formation in corpora lutea of early (days 16–19 of a normal 28 day cycle), mid (days 20–22) and late (days 23–27) luteal phases. This stimulation was inhibited by PGF_2α (10 μg/ml) in corpora lutea of mid and late luteal phases. PGF_2α alone did not show a consistent effect on basal progesterone production. The inhibition of hCG stimulated progesterone production by PGF_2α at times corresponding to luteolysis indicates a role for that prostaglandin in the process of luteolysis in the human corpus luteum.     

Fine structure of the corpus luteum of the autografted ovary in the rat

Summary The rat ovary has been transplanted successfully to subcutaneous tissue areas by several investigators. Light microscopy has revealed that corpora lutea in ovarian autografts are formed by luteinization of intact follicles and contain entrapped ova. In the present study, corpora lutea from autografted ovaries in castrate rats were obtained at metestrus and examined electron microscopically to determine whether their cellular morphology correlated with the normal progesterone levels in these animals. Cellular features usually accepted as regressive were apparent. The findings suggest either structural luteolysis is occurring before functional luteolysis or that the adrenal has increased steroidogenic activity in the castrate with ovarian autografts to account for the normal progesterone levels.Supported in part by USPHS Grant T01-DE00241-04The authors wish to thank J. Canale and Y. Tablada for technical, G. Kerimian for photographic, and M.A. Anderson for secretarial assistance     

Induction of ovulation and fertilization in the 90-day-old ewe lamb.

The induction of ovulation and fertilization was studied in 50 sexually immature crossbred ewe lambs which received 500 or 1000 i.u. PMSG with or without pretreatment with progesterone. Pretreatment with progesterone did not significantly affect ovulation, fertilization or ova recovery rates. Also, progesterone pretreatment did not significantly affect weight of the ovaries, corpora lutea, follicular fluid or the reproductive tract. Lambs receiving 1000 i.u. PMSG had a significantly (P<.05) higher ovulation rate (13.2) than lambs receiving 500 i.u. PMSG (3.4). Weights of the ovaries, corpora lutea, follicular fluid and the reproductive tract were significantly (P<.05) higher in ewes receiving 1000 i.u. PMSG. None of the lambs exhibited estrus when checked daily following HCG injection. The low ova recovery rate (16 to 38 percent) was postulated to be due to failure of the fimbria of the influndibulum to surround the enlarged stimulated ovary and pick up released ova.     

Effects of systemic administration of indomethacin to cyclic ewes on endometrial concentrations of prostaglandins effects on estrous cycle length and on progesterone, luteinizing hormone and prolactin patterns

Experiments were designed to evaluate in cyclic sheep the effects of systemic administration of a prostaglandin synthetase inhibitor (Indomethacin). Indomethacin (100 mg, 3 times daily, S.C.) was administered from day 7 of the estrous cycle for 16 days to five ewes in which the cycle was synchronized as well as the cycles of five control ewes. All control ewes had cycles of approximately 17 days duration, but three of five Indomethacin treated ewes showed no estrous behavior before their slaughter at 23 days after induced ovulation. Autopsy revealed normal corpora lutea which had not undergone luteolysis, as confirmed by progesterone determination in blood. The two remaining Indomethacin treated ewes showed an estrous behavior on day 19 and 20 respectively together with a "preovulatory surge" of luteinizing hormone and prolactin which was not followed by follicular rupture. These results show that inhibition of PGF2 alpha synthesis by systemic administration of Indomethacin to the ewe is able to prevent luteolysis. When luteolysis did occur however, it was not followed by an ovulation despite a normal gonadotropin surge, indicating that inhibition of prostaglandin synthesis by systemic administration of Indomethacin interferes with the luteolysis and follicle rupture processes.     

Reactivation of regressing corpora lutea by estradiol in the pregnant rat: dependence on placental lactogen

Previous investigations have clearly demonstrated that estradiol maintains corpus luteum function. However, it is unknown whether estradiol can restimulate progesterone synthesis and/or growth of corpora lutea that have already undergone luteolysis. The present study was designed to determine 1) whether estradiol can reactivate the steroidogenic capacity and/or growth of corpora lutea that are deprived of luteotropic support, 2) whether estradiol affects progesterone metabolism, and 3) whether the action of estradiol is related to levels of rat placental lactogen in the peripheral circulation. Rats were hypophysectomized and hysterectomized on Day 12 of pregnancy and were treated between Days 12 and 15 with either estradiol (100 micrograms/day) or 1-cm testosterone implants. Both treatments are known to maintain luteal concentrations of estradiol at physiological levels. In vivo treatment with either estradiol or testosterone prevented the drop in progesterone production and maintained the concentration of serum progesterone at levels found in intact pregnant rats. This action was not due to an alteration in the rate of metabolism of progesterone to 20 alpha-hydroxyprogesterone, since peripheral serum levels and in vitro production of 20 alpha-hydroxyprogesterone were unaffected by estradiol. When testosterone treatment was started 24 and 48 h after hypophysectomy and hysterectomy, at a time when progesterone production had been markedly reduced and luteal growth had ceased, a restimulation of both progesterone synthesis and luteal growth was observed. However, in all cases the ability of estradiol to stimulate progesterone was finite, and corpora lutea ceased to respond by Day 17, coincident with the time that rat placental lactogen became undetectable in the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Trophoblastic factors and the maternal recognition of pregnancy in sheep and cattle

The establishment of pregnancy in domestic ruminants depends upon the continued secretion of progesterone by the corpora lutea. In non-pregnant cycles the corpora lutea regress between days 12-15 after oestrus in the sheep; this process must be blocked to ensure continued exposure of the uterus to progesterone. This review discusses the evidence that embryonic products are involved in the maintenance of corpus luteum function, the identification of factors which may be responsible for this maintenance and the probable mechanism of action. The discussion centres on the recent identification of a trophoblast interferon which is thought to be the major trophoblastic factor preventing luteolysis in sheep and cattle.     

Consequences of increasing or decreasing plasma FSH concentrations during the preovulatory period in Romney ewes

Romney ewes were infused with ovine FSH (NIADDK-oFSH-16) for 48 h from the initiation of luteolysis with cloprostenol. Doses of 2.5 or 5 micrograms/h which partly or completely prevented the normal preovulatory decline in plasma FSH concentrations caused a significant increase in mean ovulation rates. Ovulation rates were not increased significantly if the FSH (5 micrograms/h) was infused for only 20 h starting from the initiation of luteolysis or 24 h later. Infusion of a less potent and relatively impure preparation of FSH (i.e. FSH-P) at 0.5 mg/h for 48 h after cloprostenol treatment also increased the mean ovulation rate significantly. However, if the FSH-P was given for only the first 24 h, or if the start of the infusion was delayed for more than 12 h, mean ovulation rates were not increased significantly. Infusion of LH (NIADDK-oLH-25, 5 micrograms/h) for 48 h from the initiation of luteolysis decreased the mean ovulation rate significantly. Administration of bovine follicular fluid to suppress plasma FSH concentrations below normal during the first 24 h after cloprostenol injection did not delay oestrus. However, oestrus was delayed by approximately 2 days if plasma FSH concentrations were reduced by bovine follicular fluid 24 h after the initiation of luteolysis. As ovulation rate increased, the mean weight of individual corpora lutea of each ewe decreased. In ewes with a single ovulation, most corpora lutea weighed greater than 600 mg, but as the ovulation rate increased the proportion of corpora lutea present weighing less than 400 mg rose steadily.(ABSTRACT TRUNCATED AT 250 WORDS)     

Function of abnormal corpora lutea in vitro after GnRH-induced ovulation in the anoestrous ewe

Normal and abnormal corpora lutea were recovered from anoestrous Romney Marsh ewes on Days 3, 4, 5 and 6 after treatment with small-dose (250 ng) multiple injections of GnRH followed by a bolus injection (125 micrograms) with (+P) and without (-P) progesterone pretreatment and a study made of their characteristics in vitro. Plasma progesterone concentrations initially rose concurrently in all animals but abnormal luteal function occurred in 70% of the -P ewes and was defined on Day 5 when plasma progesterone concentrations declined relative to those in the +P ewes. All corpora lutea recovered on Days 3 and 4 appeared macroscopically similar and there were no significant differences between the +P and -P groups in terms of luteal weight, progesterone content and binding of 125I-labelled hCG on these days. However, corpora lutea from the -P animals only exhibited a decline in progesterone production in vitro on Day 4 (P less than 0.01), and morphological differences became apparent on Days 5 and 6 when the abnormal corpora lutea from the -P animals also decreased in weight (P less than 0.01) and progesterone content (P less than 0.001). Binding of 125I-labelled hCG increased on Day 5 in the normal corpora lutea only. These results show that, although abnormal luteal function induced by GnRH treatment of anoestrous ewes could not be distinguished from normal corpora lutea before Day 5 by measurement of progesterone in peripheral plasma, a significant decline in progesterone production in vitro occurred on Day 4 in the abnormal corpora lutea. This was followed by significant decreases in weight and progesterone content and a failure to increase 125I-labelled hCG binding. Abnormal corpora lutea are therefore capable of some initial growth and progesterone production, before undergoing a rapid and premature regression from Day 4, which has similar characteristics to natural luteolysis.     

Effect of RU 486 on luteal function in the early pregnant rat

A dose of 30 mg RU 486/kg, an antiprogesterone, was administered to pregnant rats on Day 2 (Group 1) or Day 4 (Group 2) of pregnancy. RU 486 significantly changed serum progesterone and oestradiol concentrations and luteal 3 beta-HSD and 20 alpha-HSD activities in Group 1, and implantation was significantly inhibited. The luteal 3 beta-HSD activity in Group 2 rats on Day 6 was significantly (P less than 0.01) lower than the control value (7.5 +/- 0.6 and 10.1 +/- 0.6 mU/mg protein respectively). This decline in the 3 beta-HSD activity was followed by a marked decrease in the serum progesterone concentration, resulting in a significant decrease of the progesterone/oestradiol ratio and implantation was completely inhibited. The 20 alpha-HSD activity, which could not be detected on Day 6 in the control rats, was twice as great in Group 2 than in Group 1 rats (17.5 +/- 1.2 and 7.4 +/- 3.1 mU/mg protein respectively). Ultrastructural examination of corpora lutea of Group 2 rats confirmed luteolysis. These results suggest that RU 486 has a luteolytic effect and its anti-implantation effect is concomitant with luteolysis of the corpora lutea of pregnancy.     

Effects of systemic administration of indomethacin to cyclic ewes on endometrial concentrations of prostaglandins effects on estrous cycle lenght and on progesterone, luteinizing hormone and prolactin patterns

Experiments were designed to evaluate in cyclic sheep the effects of systemic administration of a prostaglandin synthetase inhibitor (indomethacin). Indomethacin (100 mg, 3 times daily, S.C.) was administered from day 7 of the estrous cycle for 16 days to five ewes in which the cycle was synchronized as well as the cycles of five control ewes. All control ewes had cycles of approximately 17 days duration, but three of five Indomethacin treated ewes showed no estrous behavior before their slaughter at 23 days after induced ovulation. Autopsy revealed normal corpora lutea which had not undergone luteolysis, as confirmed by progesterone determination in blood. The two remaining Indomethacin treated ewes showed an estrous behavior on day 19 and 20 respectively together with a “prevulatory surge” of luteinizing hormone and prolactin which was not followed by follicular rupture. These results show that inhibition of PGF₂α synthesis by systemic administration of Indomethacin to the ewe is able to prevent luteolysis.When luteolysis did occur however, it was not followed by an ovulation despite a normal gonadotropin surge, indicating that inhibition of prostaglandin synthesis by systematic administration of Indomethacin interferes with the luteolysis and follicle rupture processes.     

Effect of active immunization of pre-partum and post-partum cows against prostaglandin F-2 alpha on lifespan and progesterone secretion of short-lived corpora lutea

Mature beef cows were actively immunized pre partum (N = 5) or post partum (N = 10) against a PGF-2 alpha-ovalbumin conjugate or against ovalbumin alone (control; N = 5). All cows in the control group exhibited first oestrous cycles which were of short duration (less than or equal to 12 days). Mean specific serum binding to [3H]PGF-2 alpha in the control group was consistently less than 1%. In the pre-partum PGF-2 alpha-immunized cows, lifespan and progesterone secretion of the first corpus luteum formed post partum was maintained for greater than 39 days. Specific serum binding to [3H]PGF-2 alpha in pre-partum and post-partum PGF-2 alpha-immunized cows was elevated. Lifespan of the first corpus luteum formed in post-partum PGF-2 alpha-immunized cows was short (less than 10 days; N = 1), normal (mean = 22 days; N = 4) or maintained (greater than 31 days; N = 5). Luteal lifespan was dependent upon serum PGF-2 alpha antibody titres, with cows exhibiting higher titres frequently having prolonged luteal lifespans after first ovulation. We conclude that active immunization of beef cows against PGF-2 alpha extends the lifespan and progesterone secretion of corpora lutea anticipated to be short-lived. These results support the concept that the shorter lifespan of some corpora lutea in post-partum cows is due to a premature release of PGF-2 alpha from the uterus.     

In vivo intra-luteal implants of prostaglandin (PG) E(1) or E(2) (PGE(1), PGE(2)) prevent luteolysis in cows. I. Luteal weight, circulating progesterone, mRNA for luteal luteinizing hormone (LH) receptor, and occupied and unoccupied luteal receptors for LH

Previously, it was reported that chronic intra-uterine infusion of PGE(1) or PGE(2) every four hours inhibited luteolysis in ewes. However, estradiol-17β or PGE(2) given intra-uterine every 8h did not inhibit luteolysis in heifers, but infusion of estradiol+PGE(2) inhibited luteolysis in heifers. The objective of this experiment was to determine whether and how intra-luteal implants containing PGE(1) or PGE(2) prevent luteolysis in Angus or Brahman cows. On day-13 post-estrus, Angus cows received no intra-luteal implant and corpora lutea were retrieved or Angus and Brahman cows received intra-luteal silastic implants containing Vehicle, PGE(1), or PGE(2) and corpora lutea were retrieved on day-19. Coccygeal blood was collected daily for analysis for progesterone. Breed did not influence the effect of PGE(1) or PGE(2) on luteal mRNA for LH receptors or unoccupied or occupied luteal LH receptors did not differ (P>0.05) so the data were pooled. Luteal weights of Vehicle-treated Angus or Brahman cows from days-13-19 were lower (P<0.05) than those treated with intra-luteal implants containing PGE(1) or PGE(2). Day-13 Angus luteal weights were heavier (P<0.05) than Vehicle-treated Angus cows on day-19 and luteal weights of day-13 corpora lutea were similar (P>0.05) to Angus cows on day-19 treated with intra-luteal implants containing PGE(1) or PGE(2). Profiles of circulating progesterone in Angus or Brahman cows treated with intra-luteal implants containing PGE(1) or PGE(2) differed (P<0.05) from controls, but profiles of progesterone did not differ (P>0.05) between breeds or between cows treated with intra-luteal implants containing PGE(1) or PGE(2). Intra-luteal implants containing PGE(1) or PGE(2) prevented (P<0.05) loss of luteal mRNA for LH receptors and unoccupied or occupied receptors for LH compared to controls. It is concluded that PGE(1) or PGE(2) alone delays luteolysis regardless of breed. We also conclude that either PGE(1) or PGE(2) prevented luteolysis in cows by up-regulating expression of mRNA for LH receptors and by preventing loss of unoccupied and occupied LH receptors in luteal tissue.     

Effect of prostaglandin F2α on release of progesterone and leukotriene B-4 by cells from corpora lutes or mares

Corpora lutca were recovered from mares either 4 to 5 days or 12 to 13 days after ovulation. Mixed populations of luteal cells were prepared by collagenase digestion and were incubated for 24 h in the presence or absence of prostaglandin (PG) F-2 α (250 ng/ml). PGF-2 α significantly (P = 0.03) reduced progesterone secretion by cells from late diestrous corpora lutea and tended (P = 0.06) to reduce secretion by early diestrous cells. PGF-2 α had no significant effect on leukotriene B-4 (LTB-4) production by cells from early diestrous corpora lutea, but significantly (P = 0.03) increased LTB-4 production by late diestrous luteal cells. It seems possible that LTB-4 could play a role as an intermediary in the action of PGF-2 α in luteolysis in the mare.     

Seminal plasma regulates corpora lutea macrophage populations during early pregnancy in mice

In mice, exposure of the uterus to seminal plasma at mating initiates an inflammatory response within the endometrium, which is characterized by production of cytokines that recruit and activate leukocytes. We hypothesized that this seminal plasma-induced inflammatory response would extend to the ovary, increasing leukocyte abundance within corpora lutea and potentially enhancing progesterone synthesis. Female mice mated to males with their seminal vesicles surgically removed exhibited fewer macrophages within corpora lutea on the day after mating, compared with females mated to vasectomized or normal, intact males. The mean number of F4/80-positive macrophages and major histocompatibility complex (MHC) class II-positive activated macrophages was approximately 2-fold fewer in the absence of seminal vesicle fluid. The effects of seminal plasma on macrophage abundance subsided by Day 4 and were not accompanied by a change in serum progesterone levels during luteinization (Days 1, 2, or 4 after mating) or luteolysis (Days 6 or 9). In vitro secretion of progesterone from corpora lutea cultured with or without LH also did not differ between treatment groups. There was no effect of seminal plasma deficiency in males on the number of ovulated ova or corpora lutea in females. These results imply that seminal plasma exposure of the female reproductive tract at mating augments the macrophage population of newly formed corpora lutea, although these additional macrophages seem not to play a role in steroidogenesis and may instead be involved in tissue remodeling within corpora lutea.