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PubMed1980

Effect of cycloheximide on the LH release induced by a superactive analog of LH-RH.

The effect of cycloheximide on the pituitary response to a superactive analog of LH-RH (D-Ala-6-des-gly-10-LH-RH-ethylamide) was studied in intact male rats. Cycloheximide did not modify the LH release induced by the LH-RH analog within 1 hr after its injection, but produced significant supression between 1 and 4 hr. It is concluded that the early release of LH observed after the administration of the analog occurs from the readily releasable pool of LH in the pituitary gland, which is not affected by cycloheximide. The subsequent LH release that can be suppressed by cycloheximide comes from the second pool of LH.

Animals↗
PubMed1985

Studies of a controlled-release microcapsule formulation of an LH-RH agonist (D-Trp-6-LH-RH) in the rhesus monkey menstrual cycle.

It has been shown that continuous administration of LH-RH agonists inhibits ovulation in many species, including human and nonhuman primates. However, the need of daily injections or intranasal application of the LH-RH agonists makes this contraceptive approach impractical. In addition, due to the repeated daily administration of the LH-RH analogues and their bioavailability, serum levels of gonadotropins and estradiol present wide variations and are often associated with irregular bleeding and/or endometrial hyperplasia. This experiment was designed to study the effects on ovulation and the hormonal profile during the rhesus monkey menstrual cycle of a system that continuously delivers a potent agonist of LH-RH (D-Trp-6-LH-RH encapsulated in poly [DL-lactide-co-glycolide]). Subjects were divided into two groups: On day 1 of the cycle, monkeys received a single subcutaneous injection of microcapsules containing D-Trp-6-LH-RH at a release rate of 13.6 micrograms/day (Group 1) or placebo microcapsules (Group 2). Ovulation dates were significantly delayed in animals from Group 1 (50 +/- 3 days) as compared to those in group 2 (20 +/- 2 days). Luteal phases following ovulation were normal in animals of both groups, as determined by length and serum progesterone levels. No significant differences on baseline levels of FSH and LH were observed between the two groups of animals. Post-treatment cycles were ovulatory and presented normal luteal phases and hormone concentrations as compared to the non-treated animals of our colony. The present data show for the first time that a controlled-release microcapsule formulation that delivers an agonist of LH-RH can effectively suppress ovulation when injected in a single dose in non-human primates.

Animals↗
PubMed1985

LH-RH stimulated LH secretion in human endocrine disease.

The application of LH-RH provides means to describe the functional state of the hypothalamo-pituitary-gonadal axis and has helped to understand the regulation of gonadotropin secretion both under normal and pathological circumstances. At present, diagnostic LH-RH application appears to be most useful in patients with delayed puberty, where a biphasic response during an infusion of LH-RH excludes hypogonadotropic hypogonadism at an early clinical stage. An enhanced LH-RH induced response following exogenous intermittent LH-RH administration identifies the subgroup of hypogonadotropic patients who are suitable for subsequent LH-RH substitution therapy. In addition, subtle derangements of gonadotropin secretion have been described in a score of clinical conditions including the endocrine disorders discussed in this review. However, interesting as these observations may be theoretically, their practical value is often limited since a multitude of interfering factors, both exogenous and endogenous, results in a great variability in the obtained results, thus limiting the diagnostic value of the test in a specific patient. As of recently the clinical use of LH-RH includes its therapeutic application to replace low endogenous levels of LH-RH, whereas long-acting analogues of the natural decapeptide are employed to suppress gonadotropin secretion in an increasing field of endocrine disorders.

Adrenal Gland Diseases↗
PubMed1976

The effect of a single injection of testosterone propionate and estradiol benzoate on the LH-RH induced release of FSH and LH in the male rat.

Male adult, intact rats were treated with 1000 or 2000 mug/kg testosterone propionate (TP), 500 or 1000 mug/kg estradiol benzoate (EB) or ol. arachidis only. 30 min, 24h, 48h and 7 days later they were injected with 5 mug/kg LH-RH or saline solution. 30 min after this FSH, LH and testosterone were determined in plasma by radioimmunoassay. It is shown that pretreatment with 500 mug/kg TP enhances significantly the FSH release after LH-RH even on day 7, while the greater dose of TP does not significantly affect the release of FSH. The LH-RH induced release of LH is also increased by the pretreatment with 500 mug/kg TP, while 2000 mug/kg TP do not alter the reaction to LH-RH. EB in both doses does not influence the LH-RH induced release of FSH and LH.

Animals↗
PubMedDate not supplied

Sex steroid inhibition of LH induction of the LH receptor.

Testosterone and estrogen were tested as possible mediators of the prolactin-dependent LH induction of LH receptors in hypophysectomized adult male rats. Animals were injected s.c. with saline, prolactin (100 micrograms/day), or combinations of testosterone (1 mg/day) or estrogen (1 mg/day) and prolactin for 7 days following a 7-day period of hypophysectomy. Twenty-four hours after the last saline or prolactin injection, the animals were given a single i.p. injection of either saline or oLH (10 micrograms) to evaluate LH-induced LH receptor induction. Membrane preparations from testicular homogenates were incubated with [125I]hCG as the binding ligand for determination of the receptor response and capacity. Neither testosterone nor estrogen were able to mimic the ability of prolactin to allow LH to induce the LH receptor. However, both testosterone and estrogen significantly inhibited prolactin-mediated, LH induction of its homologous receptor.

Animals↗
PubMed1995

Characterization of site-directed antibodies to the LH receptor in functionally active gonadal cells and their differential effects on LH-stimulated signal transduction in Leydig tumour (MA10) cells.

In this study site-directed antibodies have been used to investigate the structure/activity relationships of the LH receptor in functionally active gonadal cells. Polyclonal antibodies were raised in rabbits against synthetic peptides corresponding to regions within both the extracellular N-terminal domain (antibodies 1 and 2 against residues 48-65 and 187-206, respectively) and the cytoplasmic C-terminal domain (antibody 3 against residues 622-636) of the LH receptor. Following affinity purification by chromatography on columns of immobilised peptides the antibodies were demonstrated to be peptide specific both by ELISA and by dot-blotting assays. On Western blots of membranes proteins prepared from superovulated rat ovaries, mouse Leydig tumour (MA10) cells, and rat testes, all three antibodies recognised a single broad band of apparent M(r) 95,000-100,000 corresponding to the putative LH receptor. The protein of apparent M(r) 95,000-100,000 also bound 125I-hCG on ligand blots, and binding was displaced by excess unlabelled hCG. The binding of 125I-hCG in the ligand blots was completely inhibited by excess unlabelled hCG. The two N-terminal antibodies (antibodies 1 and 2 (10 micrograms/ml)) also inhibited 125I-hCG binding to a greater extent than the C-terminal antibody (antibody 3 (10 micrograms/ml)). Antibody 1 (1 and 10 micrograms/ml) also potently inhibited the binding of 125I-hCG to MA10 cells. A lesser but still significant inhibition of binding was produced by antibody 2 (with 10 micrograms/ml), whereas at the concentrations tested antibody 3 exerted no greater inhibition than that yielded by pre-immune IgG. At 0.1 micrograms/ml antibody 1 significantly inhibited and at 10 micrograms/ml completely inhibited LH-stimulated cAMP and progesterone production by MA10 cells. With antibody 2, 10 micrograms/ml was required to give a significant inhibition, whereas neither antibody 3 nor pre-immune IgG had a significant effect. The antibodies had no effect on cAMP or progesterone production when added to the MA10 cells in the absence of LH. These results indicate that binding of antibody 1 and, to a lesser extent, antibody 2 interferes with ligand binding which consequently affects signal transduction. In view of the ability of the antibodies to recognise the LH receptors both in the ovary and the testis and in more than one rodent species, and their greater apparent potency than previously available antisera, the anti-peptide antibodies raised in the present study will therefore be useful to study LH receptors in normal, functionally active gonadal cells.

Animals↗
PubMed1998

Immunoexpression of the steroidogenic enzymes 3-beta hydroxysteroid dehydrogenase and 17 alpha-hydroxylase, C17,20 lyase and the receptor for luteinizing hormone (LH) in the fetal rat testis suggests that the onset of Leydig cell steroid production is independent of LH action.

The production of testosterone in the adult testis is mainly regulated by LH. Testosterone is essential for normal development of the male fetus. The regulation of testosterone production in the fetal testis is less clear than in the adult testis, and there are indications that at least the onset of androgen production in the fetal testis takes place in an LH-independent way. The aim of the present study was to compare the onset of synthesis and pattern of expression of LH receptors and two important steroidogenic enzymes, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17alpha-hydroxylase/17,20-lyase (P450c17), in fetal rat gonads. Whole fetuses (13.5 and 14.0 postcoitum (p.c.), testes, and ovaries dissected from fetuses on Days 14.5 p.c. to 20.5 p.c. and testes obtained on Days 3, 5, and 7 postpartum were fixed in Bouin's solution and processed for immunocytochemistry. In all samples of fetal testis, 3beta-HSD was detected on Day 14.5 p.c., and immunoexpression of P450c17 appeared one day later on Day 15.5 p.c. Thereafter, immunoexpression of both enzymes remained intense throughout gestation and postnatally. In contrast, immunoexpression of LH receptors was detectable only from Day 16.5, when a few weakly positive cells were present, but it became more intense one and two days later. Similar to the immunostaining for 3beta-HSD and P450c17, immunostaining for LH receptor remained strong throughout gestation and during the first 7 days of postnatal life. No immunoexpression of any of the three proteins studied was detected in the fetal ovary at any age. These data show very early immunoexpression of 3beta-HSD, which was detected one day before the reported start of steroid production by the fetal Leydig cells. In contrast, immunoexpression of LH receptors was evident only after immunoexpression of both the steroidogenic enzymes studied had became apparent and after the reported start of steroidogenesis, which is consistent with the theory that onset of steroidogenesis in the fetal rat testis is an LH-independent process.

3-Hydroxysteroid Dehydrogenases↗
PubMed1996

Effects of the mutations (Trp8 --> Arg and Ile15 --> Thr) in human luteinizing hormone (LH) beta-subunit on LH bioactivity in vitro and in vivo.

The mutations (Trp8 --> Arg and Ile15 --> Thr) in the human LHbeta -subunit caused by nucleotide point mutations in the LHbeta gene were reported in women with immunologically anomalous LH and menstrual disorders. To estimate the effects of the mutations on LH bioactivity in vitro and in vivo, we constructed a LHbeta gene containing this nucleotide mutation in each site or in both sites by site- directed mutagenesis and analyzed the bioactivities of the mutant LH expressed in Chinese hamster ovary cells. Although no alterations were noted in the receptor-binding activity of LH due to the mutations, the LHs containing the mutations at Trp8 --> Arg and at both sites in the beta-subunit showed a higher biopotency of progesterone production in vitro. The clearance rate from the circulation was faster in vivo in all mutant LHs, which were induced primarily by the mutation at Trp8 --> Arg. However, the mutations did not affect the ability of LH to induce ovulation in vivo. These results indicate that LH consisting of the mutant beta-subunit exhibits hyperbioactivity on steroidogenesis and has a short turnover rate. This may affect the endocrine pathway among women with the mutant LH and lead to menstrual disorders.

Animals↗
PubMed2003

Luteinizing hormone (LH)-responsive Cushing's syndrome: the demonstration of LH receptor messenger ribonucleic acid in hyperplastic adrenal cells, which respond to chorionic gonadotropin and serotonin agonists in vitro.

In a substantial part of adrenal adenomas and hyperplasias from patients with Cushing's syndrome, cortisol production is controlled by the expression of aberrant hormone receptors on adrenocortical cells. We present in vivo and in vitro data of two patients with a LH-responsive Cushing's syndrome based on ACTH-independent bilateral adrenal hyperplasia. Patients 1 and 2 are women who presented with Cushing's syndrome and bilateral adrenal hyperplasia. Endocrine testing demonstrated absence of cortisol diurnal rhythm, insufficient cortisol suppression after 1 mg dexamethasone orally, and undetectable ACTH levels in both patients. Both patients were treated by laparoscopic biadrenalectomy. In in vivo testing, in patients 1 and 2, a profound cortisol rise was found after administration of GnRH [change in cortisol (Delta F), 118 and 106%, respectively], human CG (Delta F, 133 and 44%), LH (Delta F, 73 and 43%), ACTH (Delta F, 89 and 181%), and the 5-hydroxy-tryptamine receptor type 4 (5-HT(4)) agonists cisapride (Delta F, 141 and 148%) and metoclopramide (Delta F, 189 and 95%). In in vitro testing, adrenal cells from patient 2 responded, in a dose-dependent fashion, with cortisol production after exposure to human CG (Delta F, 45%), cisapride (Delta F, 68%), and metoclopramide (Delta F, 81%). ACTH induced cortisol production by cells from both patients (Delta F, 135 and 159%). In receptor studies, LH receptor mRNA was demonstrated in adrenal tissue of both patients but also in control adrenal tissue of two patients with persisting pituitary-dependent Cushing's syndrome treated by biadrenalectomy. In neither patient were mutations found in the ACTH receptor gene. LH-responsive Cushing's syndrome associated with bilateral adrenal hyperplasia may result from aberrant (or possibly increased) adrenal LH receptor expression. This variant is further characterized by adrenal responsiveness to 5-HT4 receptor agonists, possibly pointing to an interaction between LH and serotonin in the regulation of cortisol secretion. Despite the regulatory potential of LH and 5-HT4 receptor agonists on cortisol production in our patients, their adrenals seemed to be still sensitive to ACTH, both in vivo and in vitro.

Adrenal Glands↗
PubMed1999

A limited repertoire of mutations of the luteinizing hormone (LH) receptor gene in familial and sporadic patients with male LH-independent precocious puberty.

Herein, we report mutation analysis of the LH receptor gene in 17 males with LH-independent precocious puberty, of which 8 were familial and 9 had a negative family history. A total of 7 different mutations (all previously reported) were detected in 12 patients. Among 10 European familial male-limited precocious puberty (FMPP) patients who had a LH receptor gene mutation, none had the Asp578Gly mutation, which is responsible for the vast majority of cases in the U.S. The restricted number of activating mutations of the LH receptor observed in this and other studies of FMPP strongly suggests that an activating phenotype is associated with very specific sites in the receptor protein. Clinical follow-up of the 5 patients who did not have LH receptor mutations shows that such cases most likely do not have true FMPP. LH receptor mutation analysis provides a sensitive tool for distinguishing true FMPP from other causes of early-onset LH-independent puberty in males.

Amino Acid Sequence↗
PubMed1984

Effects of LH-RH and Des-Gly10[D-Ala6]LH-RH-ethylamide on plasma sex steroid profiles in adult female coho salmon (Oncorhynchus kisutch).

17 beta-Estradiol, testosterone, and 17 alpha, 20 beta dihydroxy-4-pregnen-3-one (17 alpha 20 beta P) levels were measured in plasma samples obtained from coho salmon (Oncorhynchus kisutch) during the preovulatory period and following the injection of mammalian gonadotropin releasing hormones. Spontaneous reproductive activity was characterized by a rapid decline in plasma 17 beta-estradiol 10 days prior to ovulation and a large increase in plasma 17 alpha 20 beta P 6 days before ovulation. Testosterone levels remained high (greater than 125 ng/ml) throughout the preovulatory period, with a small peak evident 6 days prior to ovulation. Oocyte development was not accelerated in fish injected with mammalian LH-RH, whereas des-Gly10[D-Ala6]LH-RH-ethylamide (LH-RHA DAla6) promoted germinal vesicle breakdown (GVBD) in 10 out of 14 fish within 96 hr. Only LH-RHA DAla6-injected fish which completed GVBD displayed the characteristic steroid changes observed during spontaneous reproductive activity. In LH-RH-injected fish, there was a transient increase in plasma 17 alpha 20 beta P levels which persisted for less than 24 hr. LH-RHA DAla6-injected fish which failed to complete GVBD maintained high 17 alpha 20 beta P levels, but the peak concentrations were lower than those in fish which completed GVBD. These fish also maintained high plasma 17 beta-estradiol levels when compared to fish which completed GVBD. The appearance of high plasma 17 alpha 20 beta P levels during spontaneous and LH-RHA DAla6-induced reproductive activity was coincident with the time of GVBD. This finding was consistent with the view that 17 alpha 20 beta P functions as the maturation-inducing steroid in salmonids. The induction of GVBD using gonadotropin-releasing hormones was related to the elevation of plasma gonadotropin levels for greater than 24 hr [G. Van Der Kraak, H. R. Lin, E. M. Donaldson, H. M. Dye, and G. A. Hunter (1983) Gen. Comp. Endocrinol. 49, 470-476] and a decrease in 17 beta-estradiol production.

Animals↗
PubMed1989

Reversible inhibition of testicular androgen secretion by 3-, 5- and 6-month controlled-release microsphere formulations of the LH-RH agonist [D-Trp6, des-Gly-NH10(2)] LH-RH ethylamide in the dog.

This study examines the effect of treatment with controlled-release poly(DL-lactide-coglycolide) microsphere formulations of the LH-RH agonist [D-Trp6, des-Gly-NH10(2)]-LH-RH ethylamide (LH-RH-A) designed to release about 100 or 200 micrograms of the peptide per day for 3, 5 or 6 months in male dogs. Plasma levels of testosterone and LH-RH-A were measured at 2-day intervals. After the first injection of the 100-micrograms/day formulation, plasma testosterone increased from 1.6 +/- 0.2 to 3.5 +/- 0.6 ng/ml for 5-7 days before decreasing and remaining at 0.05 +/- 0.008 ng/ml for approximately 150 days (5 months). After two months of recovery, microspheres designed to release 100 micrograms for 6 months of LH-RH agonist per day were then injected. Plasma testosterone levels showed an elevation from 1.5 +/- 0.5 to 4.7 +/- 2.0 ng/ml during the first few days before gradually decreasing to castration levels for 200 days (6 months). One month later, plasma testosterone had returned to normal levels. When microspheres designed to deliver an average of 200 micrograms per day of the peptide for 3 months were injected in another series of animals, castration levels of plasma testosterone were maintained for 95 days with a progressive increase to normal values at later time intervals. The animals of the first series of experiments were then sacrificed after 4 months of recovery following maintenance of plasma testosterone at castration levels for a total period of 11 months. The testes, prostate and pituitary gland were kept for histological examination which was completely normal in all tissues. The efficacy and excellent tolerance of the controlled-release form of LH-RH-A as inhibitor of the pituitary-gonadal axis strongly support the use of such long-term controlled-release formulations of LH-RH agonists for the treatment of sex steroid sensitive diseases.

Animals↗
PubMed1996

Testosterone inhibits the basal and gonadotropin-releasing hormone-stimulated synthesis and release of newly synthesized alpha- and lutropin (LH) beta-subunit but not release of stored LH in cultured rat pituitary cells.

To further explore the mechanism of steroid feedback in male, the effects of testosterone (T) and gonadotropin-releasing hormone (GnRH) on the rates of alpha- and lutropin (LH)beta-chain synthesis, neosynthesized subunits and radioimmunoassayable LH release into the medium were studied in the cultures of anterior pituitary cells from orchiectomized and intact rats. Polypeptides were [35S]methionine-labeled, immunoprecipitated separately in the medium and cells, then after SDS-PAGE precisely quantified. The total (medium + cells) radioactivity incorporated in the absence of GnRH into alpha- and LH beta-subunit was increased in orchiectomized rat cells vs. intact rat cells. GnRH stimulated the synthesis of both subunits, whether cells were from normal or castrated rat. T suppressed basal and GnRH-enhanced synthesis of both subunits in castrated rat cells. The values became closed to those observed in the normal rat cells. Also release of neosynthesized subunits from castrated rat cells into the culture medium was inhibited by T. In contrast, T did not change the basal and GnRH-induced radioimmunoassayed LH release. These results show that T can inhibit directly, at the pituitary level, alpha- and LH beta-subunit synthesis and neosynthesized but not stored LH release. They could explain, at least in part, no correlation between modifications of GnRH and LH secretion observed in vivo in response to T replacement.

Animals↗
PubMed1992

Pituitary LH content and plasma LH levels following daily GnRH analogue treatment in male red-winged blackbirds (Agelaius phoeniceus).

1. During the 14-day treatment period, plasma LH levels following GnRH analogue (GnRH-A) injections (10.0 micrograms) were significantly reduced after the 6th and the 14th injection. 2. One day post-treatment, the LH pituitary content was significantly reduced in GnRH-A-treated redwings compared to saline-injected controls. 3. Pituitary LH content was significantly higher in GnRH-A treated birds compared to control birds 14 and 28 days post-treatment and plasma LH levels were similar in both groups. 4. Hypersecretion of LH following GnRH-A injections appears to reduce pituitary LH content, acting as a stimulus for its synthesis. 5. These results suggest a higher LH synthesis and storage in the pituitary gland of the GnRH-A-treated birds compared to the control birds during the post-treatment period.

Animals↗
PubMed1981

Inhibition of LH-release by synthetic analogues of LH-RH in rat pituitary cell culture.

Conditions for testing the inhibitory activity of synthetic analogues of LH-RH in monolayer cultures of rat pituitary cells were optimized. Nine synthetic derivatives of LH-RH were tested to evaluate their inhibitory dose50(ID50) values. The peptide antagonists tested included linear, branched-chain, dimeric and tetrameric derivatives of LH-RH, Ac-D-Phe1, D-Cpa2, D-Trp3,6-LH-RH (analogue V) was found to be the most effective competitive inhibitor of the series with an ID50 value of 6 x 10(-9)M in the presence of 10(-9) M LH-RH. The kinetics of the LH-RH-blocking action of two inhibitors were also studied. Both the linear (analogue I) and the dimeric (analogue VI) peptide showed immediate inhibition of HL-release. Prolonged inhibitory activity of the same two peptides was observed when cells were incubated with LH-Rh subsequent to preincubation with the inhibitors.

Animals↗
PubMed1980

Pituitary responsiveness to LH-RH in post-partum ewes treated with oestradiol-17 beta and failing to show a plasma LH surge.

Oestradiol-17 beta (40 micrograms intravenously) failed to elicit a surge in plasma LH levels by 13 h after administration in 64% (16 out of 25) Merino ewes about 30 days post partum in the anoestrous season. LH-RH responsiveness and LH-RH priming effect were significantly greater in these ewes than in similar post-partum (n = 9) and non-parturient ewes (n = 3) not treated with oestradiol. This suggests that the failure of the oestrogen-positive feedback effect on LH release in post-partum ewes is not due to a failure of oestradiol action on the pituitary increasing pituitary responsiveness to LH-RH and LH-RH priming effect, but could be due to inadequate release of LH-RH from the hypothalamus.

Animals↗
PubMed2004

Dose-finding study of daily GnRH antagonist for the prevention of premature LH surges in IVF/ICSI patients: optimal changes in LH and progesterone for clinical pregnancy.

BACKGROUND: An optimal range of LH concentrations for achieving pregnancy has not been established. The aim of this study was to investigate the effect of various LH levels induced by different GnRH antagonist doses on IVF outcome. METHODS: This was a prospective, single centre study including 144 IVF patients, stimulated with recombinant FSH from cycle day 2, and co-treated with daily GnRH antagonist (antide/Iturelix) (2 mg/2 ml, 1 mg/ml, 0.5 mg/ml, 0.5 mg/0.5 ml or 0.25 mg/ml) from cycle day 7 onwards. Serum samples were taken three times daily. RESULTS: Clinical pregnancies were only observed within a particular range of change in LH levels. The upper and lower thresholds for the mean LH area under the curve (AUC), adjusted for the baseline LH level before the antagonist was started (LH AUC(-S6); S6=stimulation day 6) were -2.2 and 12.4 (IU/l) respectively (a negative value=below baseline levels). There were no clinical pregnancies outside these threshold values. Similar results were found for progesterone, the threshold levels of progesterone AUC(-S6) were 3.98 and -1.21 ng/ml. Moreover, there were no pregnancies with progesterone levels >0.26 ng/ml/follicle on the day of hCG. CONCLUSIONS: Excessive or insufficient suppression of LH and progesterone levels during GnRH antagonist administration and high progesterone/follicle on hCG day seems to be associated with impaired clinical pregnancy rates.

Adult↗
PubMed2004

No evidence for pituitary priming to gonadotropin-releasing hormone in relation to luteinizing hormone (LH) secretion prior to the preovulatory LH surge in ewes.

The purpose of this study was to determine the occurrence of and the regulatory mechanisms involved in priming of the pituitary to GnRH before the preovulatory LH surge in sheep. Experiment 1: Forty-two ewes had progestagen devices removed after 14 days and were assigned to luteal (Lut) or follicular (Foll) groups. Fifteen days later, blood sampling was initiated either immediately or 36 h after induced luteolysis in groups Lut and Foll, respectively. After 4 h, ewes were administered either saline (n = 5) or 250 ng (n = 8) or 10 microg (n = 8) of GnRH. Five ewes per treatment group were killed 1 h later, while remaining animals were blood sampled for a further 7 h. Experiment 2: Eighteen ewes were allocated to Lut and Foll groups (described above). Blood samples were collected from 2 h before GnRH (10 microg) treatment until 7 h after. Despite up-regulated GnRH-R mRNA levels in Foll ewes, pituitary content and plasma levels of LH and LHbeta mRNA levels were similar between groups. Mean FSHbeta mRNA and plasma FSH levels were elevated in Lut ewes but declined after GnRH treatment. Inversely, plasma estradiol and inhibin-A concentrations were higher in Foll ewes and declined after GnRH treatment. Fewer LH(+ve)/secretogranin II(-ve) (SgII(-ve)) granules were present in gonadotropes of Foll ewes, coincident with increased basal LH levels. Fewer smaller sized granules were present after GnRH treatment. In conclusion, there was no evidence of self-priming before onset of the preovulatory LH surge. Constitutive release of LH(+ve)/SgII(-ve) granules may maintain basal LH levels while smaller sized, presumably mature granules may be preferentially released after GnRH stimulation.

Animals↗