LH Deprivation Research Articles

Evaluation of relative role of LH and FSH in restoration of spermatogenesis using ethanedimethylsulphonate-treated adult rats

Spermatogenesis is a complex process, and previous studies have clearly established the role for testosterone in its maintenance. However, the role of FSH remains controversial, although several lines of evidence suggest its importance in initiation of spermatogenesis. In the present study, the relative roles of FSH and LH have been evaluated using specific antisera capable of neutralizing endogenous hormones in adult male rats following ethanedimethylsulphonate (EDS) treatment. Restoration of spermatogenesis in EDS-treated rats was monitored following FSH or LH deprivation by histological analysis and flow cytometry. Deprivation of FSH resulted in a reduction of seminiferous tubule diameter and spermatogonial number, which was much more drastic than that observed following LH deprivation. More importantly, FSH deprivation was associated with a significant reduction in the number of pachytene spermatocytes. These results provide evidence for a definite role for FSH in regulation of spermatogenesis, in addition to confirming the role of LH in spermatogenesis via testosterone.

Dose and time relationships of intravenously injected rat recombinant luteinizing hormone and testicular testosterone secretion in the male Rat.

The ability of hCG and LH to induce testosterone (T) secretion by Leydig cells is well documented. However, the influence of the pulsatile nature of LH secretion, with varying frequency and amplitude, on T production in vivo is less clear. In our earlier studies on the relationship between pulsatile LH release and T secretion in adult male rats, no simple causality was observed. The recent availability of rat recombinant (rec) LH prompted us to study the effects of one and of three i.v. pulses of different doses of rat recLH on T secretion in adult male rats rendered hypogonadotropic by treatment with the GnRH antagonist cetrorelix. One or three supraphysiological pulses of 1.0 microg of rat recLH produced similar maximal T responses. In contrast, high physiological LH pulses (0.1 microg) produced discrete T-response peaks, whereas multiple low pulses of LH (0.03 microg) were needed before a T response was achieved. The T stimulation was greatly diminished after an LH pulse of 0.1 microg if rats had been treated on the previous day with pulses of 0.03 vs. 0.1 microg rat recLH, apparently because of prolonged LH deprivation and lack of Leydig cell priming due to the GnRH antagonist treatment. The novel preparation of rat recLH provides a physiologically relevant tool for studying the complex relationship between pulsatile LH release and T secretion in male rats.

Changes in testicular function following specific deprivation of LH in the adult male rabbit.

Sexually mature male rabbits actively immunized against highly purified ovine LH (oLH) were used as a model system to study the effects of endogenous LH deprivation (and therefore testosterone) on spermatogenesis as well as pituitary FSH secretion. Immunization against oLH generated antibody titres capable of cross-reacting and neutralizing rabbit LH and this resulted in a significant reduction (P < 0.01) in serum testosterone levels by 2-4 weeks of immunization. A significant increase in circulating FSH concentration (from a basal level of approximately 1 ng to 60-100 ng/ml; P < 0.01) was observed within 4-6 weeks of immunization, perhaps a consequence of the negative feedback effect of the lack of testosterone. The effect of LH deprivation on spermatogenesis assessed by DNA flow cytometry and histological analyses of testicular biopsy tissue revealed that lack of testosterone primarily results in a rapid reduction and complete absence of round (1C) and elongated (HC) spermatids. The immediate effect of LH/testosterone deprivation thus appears to be at the step of meiotic transformation of primary spermatocytes (4C) to 1C. A significant reduction (> 80%; P < 0.01) in the 4C population and a relative accumulation (> 90%; P < 0.01) in spermatogonia (2C) was also observed, suggesting a need for testosterone during the transformation of 2C to 4C. In all but one of the rabbits, both qualitative and quantitative recovery in spermatogenesis occurred during the recovery phase, even at a time when only a marginal increase in serum testosterone (compared with the preimmunization) levels was observed as a result of a rapid decline in the cross-reactive antibody titres. These results clearly show that LH/testosterone deprivation in addition to primarily affecting the meiotic step also regulates the conversion of 2C to 4C during spermatogenesis.

Effects of bovine follicular fluid and luteinizing-hormone-releasing hormone antagonist on the dominant follicle maintained by a norgestomet ear implant in heifers

The effects of BFF and LHRHa on the dominant follicle, maintained by 9-d synthetic progestin (norgestomet) ear implants inserted at proestrus, were studied in cattle. From day 4 of implant insertion, heifers (n = 18) were injected twice daily with saline (control, n = 6) or charcoal-extracted bovine follicular fluid, 10 mL i.v. for 4 d (BFF, n = 6) or LHRHa, 0.8 mg i.v. for 3 d (LHRHa, n = 6). Follicular changes were monitored daily by ultrasonography. Plasma estradiol-17β, serum LH and FSH were measured by radioimmunoassays. The dominant follicle was maintained during the treatment period, and it ovulated after implant removal in control heifers. In BFF group, the dominant follicle either ovulated after implant removal (two of six heifers) or gradually regressed until day 10 in the post-implant period (other four of six heifers). In the LHRHa group, the dominant follicle regressed during or after the implant period in 5 of 6 heifers. The dominant follicle ovulated in 1 of 6 heifers. Growth rate of the dominant follicle, until it reached its maximum diameter, was lower in BFF group than the control group (0.4 ± 0.1 vs 0.7 ± 0.1 mm d−1; P &lt; 0.01). Both BFF and LHRHa groups showed high regression rates in those follicles that did regress (2.2 ± 0.1 (n = 4) and 1.9 ± 0.8 mm d−1 (n = 5) respectively; P &lt; 0.01), compared with no regression in the control group. The BFF injections failed to suppress serum FSH levels consistently in all the heifers treated. LHRHa-treated heifers showed a significant decline (P &lt; 0.01) in the mean serum LH concentration. In conclusion, deprivation of LH causes atresia of the dominant follicle. Key words: Follicular fluid, LHRH antagonist, follicular dynamics, gonadotropins, estradiol-17β, ultrasound, regression

In Vivo and in Vitro Studies on the Differential Role of Luteinizing Hormone and Follicle-Stimulating Hormone in Regulating Follicular Function in the Bonnet Monkey (Macaca radiata) Using Specific Gonadotropin Antibodies1

Although a distinct need for FSH in the regulation of follicular maturation in the primate is well recognized, it is not clear how FSH controls the functionality of different cellular compartments of the follicle. It is also not evident whether there is a requirement for LH in follicular maturation in the primate. In the first part of the present study, female bonnet monkeys were administered a well-characterized ovine (o) LH antiserum to neutralize endogenous monkey LH for different periods during the follicular phase, and the effect on the overall follicular maturation process was assessed by analyzing serum estrogen (E) and progesterone (P) profiles. Neither continuous LH deprivation from Day 8 of the cycle nor deprivation of LH on any one day between Days 6 and 10 had a significant effect on serum E and P profiles and the follicular maturation process. The period for which the antiserum was effective was dependent upon the dose injected; 1 ml of the antiserum given on Day 8 blocked ovulation but not follicular maturation. To assess the effect of deprivation of LH/FSH at the cellular level, animals were deprived in vivo of LH (on Days 8 and 9 of the cycle) or of FSH (on Day 6 of the cycle) by injection of highly characterized hCG and ovine (o) FSH antisera, respectively; the in vitro responsiveness of granulosa and thecal cells isolated on Day 10 from these animals was then determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Reversal of long-term LH deprivation on testosterone secretion and Leydig cell volume, number and proliferation in adult rats

The purpose of this study was to determine whether Leydig cell volume and function could recover fully from long-term LH deprivation upon restoration of endogenous LH secretion, and whether the restoration of LH would elicit a mitogenic response, i.e. stimulate Leydig cell proliferation or affect Leydig cell number per testis. LH secretion was inhibited by treating adult rats with testosterone and oestradiol-filled (TO) silicone elastomer implants (16 weeks), and was restored by removing the implants. Changes in serum concentrations of LH and FSH, LH-stimulated testosterone secretion by testes perfused in vitro, Leydig cell volume and number per testis, average Leydig cell volume and Leydig cell [3H]thymidine incorporation were measured at weekly intervals following implant removal. The TO implants inhibited (P less than 0.01) LH secretion, but serum concentrations of FSH were not significantly different (P greater than 0.10) from control values. After implant removal, serum LH returned to control values within 1 week, whereas serum FSH increased twofold (P less than 0.01) and returned to control values at 4 weeks. LH-stimulated in-vitro testosterone secretion was inhibited by more than 99% in TO-implanted rats, but increased (P less than 0.01) to 80% of control values by 8 weeks after implant removal. The total volume of Leydig cells per testis and the volume of an average Leydig cell were 14 and 19% of control values respectively, after 16 weeks of TO implantation (P less than 0.01), but returned to 83 and 86% of controls (P greater than 0.10) respectively, by 6 weeks after implant removal. Leydig cell proliferation ([3H]thymidine labelling index) was low (less than 0.1%) in both control and TO-implanted rats, increased (P less than 0.01) fivefold from 1 to 4 weeks after implant removal and then declined to control values at 6 weeks. The increase in Leydig cell [3H]thymidine incorporation was mimicked by treating TO-implanted rats with exogenous LH, but not FSH. Leydig cells were identified in both the interstitium and the lamina propria of the seminiferous epithelium. The proportion of Leydig cell nuclei in the lamina propria was 30-fold greater (P less than 0.01) at 1 and 3 weeks after implant removal (3%) compared with that for control and TO-implanted rats (0.1%). Total Leydig cell number per testis was marginally but not significantly (P = 0.06) decreased in rats treated with TO implants for 16 weeks when compared with controls (18.4 +/- 2.2 vs 25.4 +/- 1.2 x 10(6)).(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of hypophysectomy and alterations in spermatogenic function on Leydig cell volume, number, and proliferation in adult rats.

The two major objectives of this study were to determine (i) whether the pituitary is required to maintain Leydig cell number per testis, and (ii) whether alterations in spermatogenic function in the absence of LH can affect Leydig cell volume, number, and 3H-thymidine incorporation in vivo. Four experimental treatments tested the combinations of two factors: (i) the intact pituitary vs hypophysectomy (Hypox); and (ii) arrested vs active spermatogenesis. Subdermal Silastic capsules were used to deliver a low dosage of estradiol in addition to a low dosage of testosterone (TE), which arrested spermatogenesis, or a high dosage of testosterone (HTE) which maintained active spermatogenesis. All four treatments (TE, HTE, Hypox and Hypox-HTE) inhibited LH secretion for 16 weeks. Control rats were sham hypophysectomized. Leydig cell volume per testis and the volume of an average Leydig cell decreased 70-85% (P less than 0.01 vs controls) in all treated rats, whether deprived of LH (TE) or of all pituitary secretions (Hypox), and whether spermatogenesis was arrested (TE, Hypox) or maintained by exogenous testosterone (HTE, Hypox-HTE). This result suggested that LH was the only factor required to maintain Leydig cell volume, since the absence of other pituitary factors or alterations in spermatogenic function could not override or modify the effect of LH deprivation. No significant differences were found in Leydig cell number per testis or the proportion of Leydig cells labeled with 3H-thymidine among control and experimentally treated rats. In contrast to Leydig cell volume, which depended on LH, Leydig cell number and Leydig cell division were maintained at control values in the absence of pituitary factors and spermatogenic function for 16 weeks.

Effect of long term deprivation of luteinizing hormone on Leydig cell volume, Leydig cell number, and steroidogenic capacity of the rat testis.

Leydig cells atrophy, losing cytoplasmic volume and the capacity for testosterone secretion, within 1-2 weeks of LH deprivation. We investigated the effects of long term (0-16 weeks) LH deprivation on the volume of an average Leydig cell, the volume of Leydig cells per testis, the number of Leydig cells per testis, and testosterone secretion by in vitro perfused testes. Endogenous LH was suppressed in adult rats by testosterone/estradiol-filled (TE) Silastic implants. The presence of Leydig cells in testes was verified by 1) morphological examination using light and electron microscopy, 2) histochemical localization of 3 beta-hydroxysteroid dehydrogenase activity (3 beta HSD), and 3) conversion of pregnenolone to progesterone by in vitro perfused testes. Marked quantitative differences existed in Leydig cell morphology among control and treated rats. The volume of an average Leydig cell and the total volume of Leydig cells per testis decreased (P less than 0.01) rapidly and progressively after TE implantation. At 16 weeks, the average Leydig cell lost 90% of its cytoplasmic volume and 65% of its nuclear volume. Analysis of variance failed to detect a significant decline in Leydig cell number per testis, despite a 16% reduction from the value in control rats (22.2 +/- 1.5 x 10(6)) in rats treated for 16 weeks (18.7 +/- 1.5 x 10(6)). After TE implantation, LH-stimulated testosterone secretion by in vitro perfused testes diminished (P less than 0.01) rapidly to 5% of the control values at 1 week and less than 0.3% of the control value from 4-16 weeks. In contrast, 25% of 3 beta HSD activity was retained (P less than 0.01 vs. controls) at 16 weeks, based on the rate of pregnenolone conversion to progesterone. Moreover, testes of treated rats secreted progesterone at a rate twice that of controls, when the steroid secretion rates were expressed per volume of Leydig cell cytoplasm. Loss of the testosterone-secreting capacity of testes after LH withdrawal was associated with a loss in the volume, but not a significant loss in the number, of Leydig cells. Thus, LH was required to maintain the differentiated structure and function of Leydig cells, but was not required to maintain the overwhelming majority of Leydig cells in the adult rat testis through 16 weeks. Moreover, at least one steroidogenic enzyme, 3 beta HSD, was retained by Leydig cells after long term LH deprivation.

The role of LH in regulation of leydig cell responsiveness to an LHRH agonist

The short-term relationship between deprivation of LH and changes in the responsiveness of isolated Leydig cells to an LHRH agonist was studied in adult rats injected with a potent antiserum to oLH. This treatment suppressed serum and intra-testicular levels of testosterone within 4 h of injection by 80%–90% and 70%, respectively, with further suppression to levels found in hypophysectomized rats by 20 h. At 12–20 h after antiserum injection there was no major consistent change from control values in the number of Leydig cell LH (hCG)-receptors or in the testosterone response of the cells to hCG-stimulation. In the same cells the number of LHRH-receptors and the maximal testosterone response to LHRH agonist were increased ( P < 0.001) by 50% or more, although the magnitude of increase varied considerably between experiments. The ability of LHRH agonist to enhance the testosterone response of cells to hCG-stimulation was also increased significantly ( P < 0.001) in antiserum-treated rats. Comparable changes in testosterone responsiveness to LHRH agonist were observed following purification of Leydig cells on Percoll gradients. Although there was some evidence for changes in Leydig cell LHRH-receptor numbers and responsiveness to LHRH agonist at 4 h after intravenous antiserum injection, these changes were small compared with changes seen at later times. It is concluded that Leydig cell responsiveness to an LHRH agonist is negatively regulated by LH, and this has implications with respect to a possible role of ‘testicular LHRH’ in regulation of the intra-testicular levels of testosterone.

The luteotrophic effects of estradiol and prolactin in the absence of LH in the hysterectomized, pseudopregnant rat.

The ability of estradiol and prolactin to substitute for LH as luteotrophins was investigated in Day 5 (Day 1 = ovulation)-hysterectomized pseudopregnant (PSP) rats. All animals received either a sc injection of oil, 1 pg estradiol (E-1), or 150 pg prolactin (PRL) on Day 9 in combination with either a normal horse serum (NHS) or LH antiserum (LHAS) injection. The ability of oil, E-1, or PRL to maintain luteal function was assessed by monitoring serum progesterone levels through Day 12 and their direct effects on the ovary monitored by measuring luteal and extra-luteal ovarian tissue concentrations of estradiol and progesterone on Day 12. NHS treatment in combination with either oil, E-1, or PRL main- tained elevated serum progesterone levels through Day 12 of PSP. LHAS/oil-treated rats underwent luteolysis while E-1 and PRL effectively maintained luteal function in LHAS- treated animals. PRL raised luteal and extraluteal ovarian estradiol concentrations com- pared to oil/NHS-treated controls and LHAS/oil-treated rats. E-1 induced an intraluteal rise in estradiol levels in LHAS-treated rats. While luteal progesterone concentrations fell fol- lowing oil/LHAS treatment, E-1 and PRL effectively counteracted this LHAS-induced fall. The results of these studies indicate that (i) E-1 and PRL can effectively replace LH as luteotrophins during PSP in the rat and (ii) that PRL and E-1 effectively maintain luteal levels of estradiol and progesterone following LH deprivation. It is suggested that E-1 and PRL may exert their luteotrophic actions by either an E-1-induced increase in PRL which, in turn, acts on the luteal cells to increase intraluteal estradiol concentrations, or by a direct effect of E on the corpus luteum to bypass the requirement for LH.

Acute effects of an antiserum to luteinizing hormone on ovarian steroidogenesis in the pregnant rat.

Pregnant rats were injected s.c. at 09.00 h on day 8 of pregnancy (day 1 = sperm-positive vaginal smear) with either 0.2 or 0.5 ml equine antiserum to bovine LH (anti-LH) while control rats were injected with 0.5 ml normal horse serum (NHS). Rats were decapitated 1, 3, 6, 24 and 48 h later and serum was saved for radioimmunoassay of progesterone, androstenedione, testosterone, oestrone and oestradiol. One ovary was kept for histology, and from the other, corpora lutea (three/animal) and the non-luteal ovary (ovarian remnant from which all corpora lutea were removed) were saved for steroid determinations. The production rate of steroids by the luteal and non-luteal ovarian compartment was assessed by incubation in Krebs--Ringer bicarbonate buffer for 2 h. A significant decrease in the serum concentrations of all steroid hormones was induced by 6 h after treatment with anti-LH; progesterone being the first hormone to be consistently reduced (by 3 h). The steroid concentrations remained lower than those in control rats on days 9 and 10. A single injection of anti-LH reduced the number of health antral follicles by 3 h but there were always two to four normal antral follicles per ovary on days 8-10. The initial hormonal changes in the non-luteal ovary after LH deprivation were decreases in the concentration and production rates of the androgens and oestrogens. The initial concentration of non-luteal progesterone was lower 3 and 6 h after anti-LH than in control rats. Although anti-LH induced a decrease in the serum concentration of progesterone 24 and 48 h later, the corpora lutea contained more progesterone on day 8 and produced in vitro more progesterone than controls on day 8 after 0.2 and 0.5 ml anti-LH and on day 9 when only 0.5 ml was give. The increase in the initial concentration of progesterone on day 8 probably represents accumulation resulting from inhibition of luteal progesterone release. It appears, therefore, that the initial alteration after LH deprivation is inhibition of the release of luteal progesterone and this alone is sufficient to account for the interruption of pregnancy. The in-vivo increase in luteal steroidogenesis following LH deprivation was observed to some extent with androstenedione bu testosterone was unaffected. Luteal aromatizing enzymes appeared to be very sensitive to LH deprivation on day 8 since the concentration and production of oestrogen decreased without concomitant decreases in androgen. Progesterone (4 mg) administered along with 0.2 ml anti-LH on day 8 prevented luteal regression and the corpora lutea synthesized progesterone and androgens similarly to NHS-treated controls; however, the corpora lutea of the progesterone-treated group contained and produced less oestrogen than controls.

Antiluteinizing Hormone: Acute Influence on Steroid and Gonadotropin Levels and Follicular Development in the Pregnant Hamster*

Pregnant hamsters were injected at 0900 h on day 4 or 8 (day 1 of pregnancy = sperm-positive) with 0.1 ml of either normal horse serum (NHS) or equine antibovine LH (ALH) and decapitated 1, 3, 6, 12, 18, and 24 h later. Serum was saved for RIA of FSH, PRL, progesterone (P), testosterone (T), and estradiol (E2). Corpora lutea (CL) and nonluteal ovary (NLO) were saved for steroid determinations, and one ovary was saved for histology. Regardless of the day of treatment, ALH induced an immediate decline within 1 h in the serum and luteal E2 concentrations without altering T. At 24 h after ALH, levels of T and P in CL and sera were lower than NHS controls. In NLO, T and E2 declined simultaneously within 1 h after ALH without changing P. Within the next 3–6 h, P in NLO declined to half that of NHS pregnant controls and all antral follicles showed initial signs of atresia. Collectively, these results indicate that, after LH deprivation, the initial hormonal change is a concomitant decrease of E2 in serum, CL, andLO, suggesting that LH is necessary for E2 secretion and maintenance of antral follicles in the pregnant hamster and that decreases of P in serum, CL, and NLO lag behind changes in E2. A dramatic increase in serum FSH-like material accompanied the declines in serum P and E2 after ALH treatment, suggesting that lack of steroid negative feedback at the hypothalamicpituitary axis induces hypersecretion of FSH. A large dose of ALH (0.4 ml) induced a more prompt decline in serum P than 0.1 ml ALH, indicating that a greater degree of LH deprivation may occur sooner with 0.4 ml than with 0.1 ml ALH. Unlike the hysterectomized pseudopregnant (HSP) rat, ALH on day 8 of HSP in the hamster induced a terminal decline in serum P within 24 h. In contrast, the pregnant hamster on day 8 exhibited a more gradual decline in serum P than that observed in the HSP hamster, suggesting that placental factors may be exerting luteotropic actions at this time. The results indicate that luteal aromatizing enzymes appear highly sensitive to LH deprivation since, within 1 h after ALH, luteal E2 concentrations decline without a concomitant decrease in T.

A qualitative transition in the luteotropic mechanism of early pregnancy.

Secretion of progesterone and 20α-dihydroprogesterone by dispersed rat luteal cells was studied as a function of the age of the corpora lutea from which the cells were derived and the gonadotropic hormone content of the perifusion medium employed. Progesterone secretion by luteal cells gradually declined during 5-h perifusion under conditions simulating tonic in vivo PRL-LH levels. Initial rates of progesterone secretion from cells obtained from the 5th and 8th days of pregnancy were double that from the 2nd day. Supplementation of tonic gonadotropin levels with a simulated PRL surge maintained initial progesterone secretion by day 5 cells. PRL withdrawal markedly reduced progesterone secretion, while supplemental LH was ineffective. Conversely, progesterone secretion from day 8 cells could be maintained undiminished with supplemental LH, but PRL was ineffective. Total deprivation of LH from day 8 cells resulted in acute decline of progesterone secretion. Luteal cell density of the corpora lutea increased...

Studies on Luteolysis: Effect of Antiserum to Luteinizing Hormone on Sterols and Steroid Levels in Pregnant Hamsters

The effect of luteinizing hormone antiserum (LH A/S) on sterol and steroid levels in luteal and non-luteal ovarian compartments, and on serum steroid levels of pregnant hamsters, was studied. Injection (ip) of 0.1 ml of LH A/S on day 7 caused termination of pregnancy and morphological regression of the corpus luteum (CL) within 18-20 h of treatment, whereas LH-free non-immune serum had no effect. Within 3 h of administration of LH A/S the luteal progesterone levels fell from a control value of 36.0 +/- 2.4 to 15.6 +/- 3.4 ng/mg, and estrogen from a control value of 20.8 +/- 3.4 to 12.2 +/- 1.5 pg/mg. By 12 h progesterone had dropped to 7.3 +/- 0.3 ng/mg whereas estrogen was undetectable by radioimmunoassay. Serum progesterone fell in 3 h from 5.53 +/- 0.39 to 3.15 +/- 0.26 ng/ml whereas estrogen fell from 172 +/- 26 to 123 +/- 9 pg/ml. The progesterone content of non-luteal ovarian tissue dropped in 3 h from 1.06 +/- 0.01 to 0.47 +/- 0.06 ng/mg and estrogen from 115.0 +/- 1.5 to 11.0 +/- 0.65 pg/mg. Both progesterone and estrogen were undetectable at 24 h. In the CL, free cholesterol concentration did not change significantly after A/S treatment, while esterified cholesterol increased from 2.82 +/- 0.14 to 4.14 +/- 0.25 mug/mg within 6 h and 5.52 +/- 0.17 mug/mg by 12 h. The results suggest that LH plays a critical role in the maintenance of CL of early pregnancy in the hamster and that deprivation of LH, even for periods as short as 3 h, significantly influences steroid production. The accumulation of cholesterol esters following LH-deprivation suggests that loss of cholesteryl esterase activity could be one of the events leading to luteolysis.

Effect of LH, FSH and their antisera on gestation in the hamster (Mesocricetus auratus).

Summary. When monospecific and well-characterized antiserum to highly purified ovine lh was administered to pregnant hamsters before Day 4, implantation of the ovum was inhibited. Injection of the antiserum between Days 5 and 11 resulted in termination of pregnancy. These effects were accompanied by a reduction in ovarian weights and luteal degeneration. A combination of progesterone and oestradiol-17 β were required for complete reversal of the effects of antiserum on implantation and pregnancy. The antiserum was not effective in terminating pregnancy when administered after Day 11. Injection of antiserum to ovine fsh did not alter the course of gestation. Of the three gonadotrophins (fsh, lh and prolactin) administered, only the fsh—lh combination could postpone parturition. From these observations, it can be concluded that deprivation of lh essentially affects luteal function in the pregnant hamster.