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PubMed2002

Luteinizing hormone and luteinizing hormone-releasing hormone secretion is under locus coeruleus control in female rats.

It has been suggested that norepinephrine (NE) from the locus coeruleus (LC) plays an important role in triggering the preovulatory surge of gonadotropins. This work intended to study the role of LC in luteinizing hormone (LH) secretion during the estrous cycle and in ovariectomized rats treated with estradiol and progesterone (OVXE(2)P) and to correlate it with LH releasing hormone (LHRH) content in the medial preoptic area (MPOA) and median eminence (ME). Female rats on each day of the estrous cycle and OVXE(2)P were submitted to jugular cannulation and LC electrolytic lesion or sham-operation, at 09:00 h. Blood samples were collected hourly from 11:00 to 18:00 h, when animals were decapitated and their brains removed to analyze LC lesion and punch out the MPOA and ME. Plasma LH levels and LHRH content of MPOA and ME were determined by radioimmunoassay. During metestrus, diestrus and estrus, LC lesion did not modify either LH plasma concentrations or LHRH content, but completely abolished the preovulatory LH surge during proestrus and the surge of OVXE(2)P. These blockades were accompanied by an increased content of LHRH in the MPOA and ME. The results suggest that: (1). LC does not participate in the control of basal LH secretion but its activation is essential to trigger spontaneous or induced LH surges, and (2). the increased content of LHRH in the MPOA and ME may be due to a decreased NE input to these areas. Thus, LC activation may be required for depolarization of LHRH neurons and consequent LH surges.

Animals↗
PubMed1997

Progesterone blockade of a luteinizing hormone surge blocks luteinizing hormone-releasing hormone Fos activation and activation of its preoptic area afferents.

Progesterone is capable of facilitating or blocking the luteinizing hormone (LH) surge, depending on the timing of its administration. However, the precise targets of progesterone's actions are unknown. Since recent studies described the presence of a periventricular preoptic area (pePOA) neuron population afferent to LH-releasing hormone (LHRH) neurons that is co-activated to express c-Fos with LHRH neurons at the time of the LH surge, the present study was designed to determine if the pePOA neurons contain progesterone receptors (PRs) and whether progesterone inhibition is manifested by a failure of LHRH and pePOA neurons to become activated at the time of an LH surge. For progesterone facilitation, a group of immature rats each received a silastic capsule (1.57 mm i.d., 3.18 mm o.d., 1.5 cm long) containing estradiol-17beta (E2) in peanut oil (150 microg/ml) at 09.00 h on postnatal day 28 followed 24 h later by a progesterone implant (crystalline, 1.57 mm i.d., 3.18 mm o.d., 1.5 cm long). For progesterone inhibition, a second group of rats received the estrogen capsule and a progesterone capsule (3.35 mm i.d., 4.65 mm o.d., 3.0 cm long) together at 09.00 h on day 28, and 24 h later received only a blank capsule. On the afternoon of postnatal day 29, all animals were anesthetized and perfused for localization of c-Fos and LHRH, PRs alone, or c-Fos and PRs. The present studies determined that following a progesterone-inhibition paradigm, along with blockade of the LH surge, both activation of LHRH and pePOA neurons was low or absent. Staining of PRs in progesterone-facilitated and progesterone-inhibited rats indicated that the pePOA neurons contained PRs in similar patterns. Double labeling of c-Fos and PRs in progesterone-facilitated rats indicated that nearly all the c-Fos-positive neurons of the pePOA (80 +/- 4.2%) co-expressed PRs; in progesterone-inhibited rats, only 32 +/- 12% of few c-Fos-positive neurons also contained PRs. In no instance were LHRH neurons found to contain PRs. Taken together, these data suggest that both progesterone facilitation and inhibition likely involve direct actions of progesterone on the pePOA neurons, and are consistent with a role for the pePOA neurons in transducing steroid effects on LHRH neurons.

Animals↗
PubMed1976

The effect of repeated injections of synthetic luteinizing hormone-releasing hormone on the response of plasma luteinizing hormone and follicle-stimulating hormone in young hypogonadotropic-hypogonadal patients.

Sixteen patients, ages 14 to 18, eleven with isolated gonadotropin deficiency and five with sporadic multiple pituitary hormone deficiency, were subjected to a course of five daily intramuscular injections of synthetic luteinizing hormone releasing hormone (LH-RH), 100 mug/day. Before and after the course of intramuscular injections, a rapid LH-RH test (by a one-bolus intravenous injection of 50 mug/sq m) was performed and the responses of plasma LH and follicle-stimulating hormone were measured by a radioimmunoassay method. The patients could be divided into three groups according to the response of the plasma LH to the second LH-RH test: group A, five patients with a significantly higher response of plasma LH to the second LH-RH test: group B, nine patients with a less significantly higher response of the plasma LH to the second LH-RH test; and group C, two patients with very low or no response to either stimulation used in this study. The patients in the three groups may represent different etiologic entities, namely that of a separate hypothalamic lesion, a "mixed" pituitary and hypothalamic lesion, and a "pure" pituitary lesion, respectively. It is concluded that the proposed procedure provides a useful tool for discriminating etiologic groups in patients with abnormal gonadotropic secretion. Recognition of tertiary hypogonadism (primary, pure, hypothalamic gonadotropin-releasing hormone deficiency) is of practical importance in selecting those patients who can benefit from long standing LH-RH therapy.

Adolescent↗
PubMed1976

Levels of luteinizing hormone in semen of fertile and infertile men and possible significance of luteinizing hormone in sperm metabolism.

Luteinizing hormone (LH) levels were measured in the seminal plasma of 68 fertile and infertile men. LH levels in the seminal plasma were severalfold higher than those normally found in serum and were significantly higher in oligospermic and normospermic samples than in azoospermic samples. However, no significant difference was observed in LH levels of oligospermic and normospermic men. The effects of LH on fructose utilization, glucose oxidation, and adenyl cyclase activity of spermatozoa were also examined. The results indicate a possible role of seminal plasma LH in sperm motility and metabolism.

Adenylyl Cyclases↗
PubMed1981

Interpretation of plasma luteinizing hormone assay for the collection of mature oocytes from women: definition of a luteinizing hormone surge-initiating rise.

Analysis of plasma luteinizing hormone (LH) assays (4 assays per day) permits the discernment of the onset of the physiologic effects of ovulatory release. This threshold value of LH plasma concentration (LH surge-initiating rise, LH SIR) is determined for each cycle in terms of the average baseline level of the previous day. The chronology of follicle and oocyte maturation after LH SIR is similar to that which follows chorionic gonadotropin (hCG) administration: none of the 20 patients, compared with 2 out of 10, had ovulated when laparoscopy was performed 30 to 35 hours and 36 to 38 hours after LH SIR time, respectively; 1 out of 3, 9 out of 14, and 5 out of 5 patients had an in vitro fertilized egg when oocytes were collected 30 to 32, 33 to 35, and 36 to 38 hours after LH SIR time, respectively. Thus the oocyte can be collected 34 to 35 hours after the LH SIR; at this point ovulation has not occurred and the oocyte is capable of being fertilized.

Adult↗
PubMed1984

Clinical validation of enzymeimmunoassay of human luteinizing hormone (hLH) in the detection of the preovulatory luteinizing hormone (LH) surge in urine.

The preovulatory luteinizing hormone (LH) surge (mean, 60.7 standard error +/- 4.7 mIU/ml) as determined by a solid-phase enzymeimmunoassay in urine has been correlated with clinical parameters in 24 women. In group A, of seven women, the preovulatory LH surge correlated with basal body temperature and cervical mucus. In one of the women in group A, serum levels of pituitary and gonadal hormones confirmed ovulation. In group B, of 17 women, the urinary estrone-3-glucuronide (E1-3-G) peak was either coincident with or preceded the LH surge. The LH surge in all cases occurred 12 to 24 hours prior to follicular rupture, as visualized by real-time sonography. The enzymeimmunoassay for the detection of the preovulatory LH surge is useful in patients for artificial insemination and for aspiration of mature oocytes for in vitro fertilization.

Adult↗
PubMed1984

Evaluation of oxytocin administration on luteinizing hormone and follicle-stimulating hormone response to luteinizing hormone-releasing hormone during the menstrual cycle of normal women.

In order to determine whether oxytocin modifies luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion in response to LH-releasing hormone (LH-RH), a group of normal women, 23 to 30 years of age, was studied in the follicular, periovulatory, and luteal phases. LH and FSH response to LH-RH was evaluated in the serum under control conditions and after oxytocin infusion. Oxytocin administration failed to modify LH and FSH release induced by LH-RH. These results suggest that this neuropeptide is not involved in the control of LH and FSH at the level of the anterior pituitary.

Adult↗
PubMed1985

The effects of single-dose luteinizing hormone-releasing hormone on ovulatory menstrual function: support for a single luteinizing hormone- and follicle-stimulating hormone-releasing factor.

Ten ovulatory women were followed with gonadotropin and steroid determinations through two cycles. They were given 500 micrograms of luteinizing hormone-releasing hormone (LH-RH) during the periovulatory period of the second cycle to determine whether ovulation could be facilitated without altering corpus luteum function. Successive cycles demonstrated concordance for patterns of gonadotropin and steroid secretion when studied as group means. Two control cycles and one treatment cycle were consistent with luteal phase defects. The use of a supramaximal dose of LH-RH in these women neither facilitated ovulation nor adversely affected luteal function. A significant linear correlation was noted between peak LH and follicle-stimulating hormone (FSH) values for the spontaneous surges. This same linear relationship was maintained for the LH and FSH responses to 500 micrograms LH-RH. The present data produce further evidence demonstrating that the secretion of LH and FSH appears to be modulated by gonadal steroids and under the permissive control of a single gonadotropin-releasing hormone.

Adolescent↗
PubMed2001

Luteinizing hormone-dependent activity and luteinizing hormone-independent differentiation of rat fetal Leydig cells.

Addition of 5x10(-2) U/ml recombinant luteinizing hormone (LH) to testes from fetuses at 16.5 day post conception (dpc) cultured for 5 days increased the number of Leydig cells by 34% and the acute LH-stimulated testosterone production by 600%. To determine whether these positive effects of LH in vitro are physiologically relevant in vivo, fetuses were decapitated on days 16.5 pc (before the onset of LH expression in the hypophysis) or 18.5 pc (before the surge of LH in the fetal plasma) and removed at 21.5 dpc. The number of fetal Leydig cells per testis and the acute LH-stimulated testosterone production by the testes ex vivo were unaltered by decapitation. Since, in all groups, the number of Leydig cells doubled between 16.5 and 18.5 dpc and between 18.5 and 21.5 dpc, these results suggest that neither the appearance of new fully differentiated fetal Leydig cells nor the maintenance of differentiated functions in existing fetal Leydig cells depend on LH during late fetal life, although this hormone is present in the plasma. Decapitation reduced the testosterone concentrations in the plasma (-56%) and in the testis in vivo (-67%) and the basal testosterone secretion of the testis ex vivo (-70%). This suggests that LH is required to maintain the physiological activity of the Leydig cell during late fetal life. However, the decrease of the in vivo testosterone production after decapitation was not sufficient to impair the growth of the Wolffian ducts and the lengthening of the anogenital distance. In conclusion, during late fetal life in the rat, Leydig cells are LH-independent for their functional differentiation and LH-dependent for their activity.

Animals↗
PubMed2002

Transgenic and knockout mouse models for the study of luteinizing hormone and luteinizing hormone receptor function.

The main functions of luteinizing hormone (LH) are concerned with regulation of gonadal function, and these functions are today well delineated through previous physiological studies. However, novel information of less well-known aspects of actions of this hormone is currently emerging from studies on genetically modified mouse models, with either enhanced or suppressed LH/LH receptor (LHR) function. The novel functions of LH include its role, in specific situations, as promoter of formation and growth of gonadal and extragonadal tumors. Chronically elevated LH levels in transgenic (TG) mice can also induce responses to this hormone in extragonadal tissues. The knockout (KO) mouse for the LHR has elucidated various less well-known details in the function of LH during ontogeny and adult life. Finally, studies on LHR promoter function have revealed that the expression of this gene occurs in age, sex and tissues-specific fashion. The purpose of this brief review is to summarize some of our recent findings upon studies of TG and KO mice with altered function of LH or its receptor.

Animals↗
PubMed1999

Cloning and expression of cynomolgus monkey (Macaca fascicularis) gonadotropins luteinizing hormone and follicle-stimulating hormone and identification of two polymorphic sites in the luteinizing hormone beta subunit.

The genes encoding the cynomolgus monkey gonadotropin subunits, alpha, follicle-stimulating hormone (FSH) beta and luteinizing hormone (LH) beta, were cloned by reverse transcriptase polymerase chain reaction (RT-PCR) using pituitary RNA. The predicted amino acid sequences displayed 82, 96 and 87% identity to human subunit sequences, respectively. Northern blot hybridization of monkey tissues revealed pituitary specific transcripts of 1.0 and 0.6 kb for the alpha and LHbeta subunit, respectively, and two bands of 1.8 and 0.65 kb for the FSHbeta. Upon sequencing LHbeta cDNAs from different monkeys, two polymorphic sites were detected, resulting in the amino acid transitions Ser32Thr and His60Arg. Restriction analysis revealed different homo- and heterozygous combinations of the polymorphic sites indicating linkage dysequilibrium. Transient co-expression of the alpha subunit together with the FSHbeta or LHbeta subunit in COS7 and CHO cells resulted in secretion of in vitro bioactive hormones. This work represents a further step towards production of recombinant monkey LH and FSH which can be used in a homologous experimental setting in the cynomolgus monkey.

Amino Acid Sequence↗
PubMed1986

Luteinizing hormone stimulates the formation of inositol trisphosphate and cyclic AMP in rat granulosa cells. Evidence for phospholipase C generated second messengers in the action of luteinizing hormone.

The following studies were conducted to determine whether luteinizing hormone (LH), a hormone which increases cellular levels of cyclic AMP, also provokes increases in 'second messengers' derived from inositol lipid metabolism (i.e. inositol phosphates and diacylglycerol). Rat granulosa cells isolated from mature Graafian follicles were prelabelled for 3 h with myo-[2-3H]inositol. LH provoked rapid (5 min) and sustained (up to 60 min) increases in the levels of inositol mono-, bis, and trisphosphates (IP, IP2 and IP3, respectively). Time course studies revealed that IP3 was formed more rapidly than IP2 and IP following LH treatment. The response to LH was concentration-dependent with maximal increases at LH concentrations of 1 microgram/ml. LiCl (2-40 mM) enhanced the LH-provoked accumulation of all [3H]inositol phosphates, presumably by inhibiting the action of inositol phosphate phosphatases. The effectiveness of LH, however, was dependent on the concentration of lithium employed; maximal increases in IP were observed at 10 mM-LiCl, whereas maximal increases in IP2 and IP3 were observed at 20 mM- and 40 mM-LiCl, respectively. The stimulatory effects of LH on inositol phosphate and progesterone accumulation were also compared with changes in cyclic nucleotide levels. LH rapidly increased levels of inositol phosphates, progesterone and cyclic AMP, but transiently reduced levels of cyclic GMP. These results demonstrate that LH increases both cyclic AMP and inositol trisphosphate (and presumably diacylglycerol) in rat granulosa cells. Our findings suggest that two messenger systems exist to mediate the action of LH in granulosa cells.

Animals↗
PubMed2003

Suppression of pulsatile luteinizing hormone secretion but not luteinizing hormone surge in leptin resistant obese Zucker rats.

The adipose tissue-derived hormone leptin may be a primary mediator linking nutritional status and reproduction. The present study used the leptin-resistant obese female Zucker rat to investigate whether leptin signalling is required for normal pulsatile luteinizing hormone (LH) secretion and/or generation of the LH surge. For the pulsatile LH secretion study, an indwelling atrial catheter was implanted and a low dose of oestrogen given as a subcutaneous implant to lean and obese ovariectomized (OVX) Zucker rats. One week following OVX, blood samples were collected every 10 min for 3 h during the morning. Plasma LH concentrations were measured by radioimmunoassay. For the LH surge study, lean and obese OVX rats were given a high dose of oestrogen as a subcutaneous implant. Two days later, rats were given progesterone at 09.00 h to induce a proestrus-like LH surge. Blood samples were collected from an indwelling atrial catheter throughout that and the following day and plasma LH concentrations were measured by radioimmunoassay. LH pulse amplitude and mean LH secretion were profoundly attenuated in obese Zucker rats compared with lean littermates, whereas LH pulse frequency was not significantly different between phenotypes. The opioid receptor antagonist naloxone did not affect the pattern of pulsatile LH secretion in obese rats, suggesting that leptin does not exert its facilitatory effects on LH secretion through an opioidergic pathway. Both lean and obese rats showed characteristic steroid-induced LH surges. It therefore appears that a leptin signal is required for generation of a normal pattern of pulsatile LH secretion, but is not a necessary component of the steroid-induced LH surge.

Animals↗
PubMed1990

Luteinizing hormone-releasing hormone neurons express Fos protein during the proestrous surge of luteinizing hormone.

The ability of luteinizing hormone-releasing hormone (LHRH) neurons to express the oncogene c-fos was examined during the estrous cycle in rats. The immunocytochemical localization of the c-fos-encoded antigen, Fos, was coupled with the immunocytochemical localization of LHRH. LHRH neurons showed no Fos immunoreactivity during diestrus-1, diestrus-2, estrus, or the morning of proestrus. However, Fos was expressed in LHRH neurons from 1600 to 2200 hours during proestrus. The timing of onset of Fos expression in LHRH neurons during proestrus suggests a strong correlation with increased LH secretion. Pentobarbital, which blocks the preovulatory LH surge, blocked Fos expression in LHRH neurons, but the LHRH neurons expressed Fos on the following afternoon at the time of the expected delayed LH surge. Not all LHRH neurons expressed Fos during the LHRH surge. Approximately half of the LHRH neurons were activated in the preoptic area and anterior hypothalamus; more anteriorly positioned LHRH neurons did not express Fos, resulting in an overall stimulation of 40% of the LHRH neurons. These data provide direct evidence that stimulation of LHRH neurons during proestrus takes place at the LHRH cell bodies, and identify the specific population of LHRH neurons which are activated.

Animals↗
PubMed1985

Luteinizing hormone beta-subunit mRNA amounts increase during the preovulatory surge of luteinizing hormone in the ewe: the highest levels are observed at the completion of the peak.

Amounts of mRNA for luteinizing hormone (LH) beta-subunit were assessed during selected times in the normal estrous cycle of sheep. These times spanned the luteal phase through the preovulatory LH surge, and included groups designated as: (i) day 12 of the cycle (day 12); (ii) 24 hr before the onset of the expected behavioral estrus (E - 24); and (iii) 5, 15, and 25 hr after the onset of behavioral estrus (E + 5, E + 15 and E + 25). These groups were characterized by criteria such as serum and pituitary LH concentrations, serum progesterone, and ovarian morphology. Specific LH beta-subunit mRNA was evaluated by Northern transfers, using a specific bovine LH beta cDNA probe. Slopes were determined using a linear regression analysis and then expressed as fold stimulation relative to the values for the day 12 group. The results indicate that LH beta mRNA amounts increase after day 12, reaching a value of approximately 12-fold by E + 25. When correlated with serum and pituitary LH amounts, it is observed that the amounts of beta mRNA increase in a fashion parallel to serum and pituitary LH concentrations through the time E + 5. After this time, LH beta mRNA amounts continue to increase despite a dramatic fall in both serum and pituitary LH. These results suggest that LH beta mRNA amounts are regulated during the LH preovulatory surge.

Animals↗
PubMed1983

Release of progesterone from perifused, highly luteinized ovarian cells of rats: effects of luteinizing hormone and bovine serum albumin.

Release of progesterone from enzymatically dispersed luteal cells of superovulated rats was studied using a multi-channeled perifusion system. Cells were perifused with protein-free medium for up to 5 h. Basal release of progesterone showed a steady decline during the first h of perifusion to a stable baseline where it remained throughout the experiment. A 30-min exposure of the luteal cells to increasing amounts of luteinizing hormone (LH) stimulated a dose-dependent increase in progesterone release. Similar results were observed when luteal cells were exposed to 0.2 or 1.0 mM dibutyryl (Bu)2 cAMP for 30 min. Exposure of the cells to 0, 1, 10, and 100 ng LH/ml protein-free medium for 230 min showed increased release of progesterone, although the dispersed cells perifused with 100 ng LH/ml protein-free medium were unable to maintain the maximal levels of progesterone release. The effect of bovine serum albumin (BSA) in the perifusion medium on the basal and LH-stimulated progesterone release was examined. Low concentrations of BSA (0.05%) had no effect, but 0.5% and 2.0% BSA significantly increased the basal release of progesterone. However, the addition of 0.05% BSA to the medium resulted in an increased progesterone release in response to 10 ng LH/ml medium. These results suggest that the in vitro perifusion system maintains physiologically viable cells which are responsive to either LH or (Bu)2 cAMP for at least 5 h. The effect of protein in the perifusion medium or progesterone release was demonstrated by the addition of BSA.

Animals↗
PubMed1984

Effects of luteinizing hormone, progesterone, testosterone, estradiol and corticosterone on ovulation and luteinizing hormone release in hens treated with aminoglutethimide.

Aminoglutethimide (AG), an inhibitor of steroidogenesis, was administered s.c. to 5 groups of laying hens at a dose of 200 mg AG/kg body weight 9 h before expected midsequence ovulation. This dose has previously been demonstrated to consistently block ovulation. The injection of AG was followed by s.c. injections of: Group 1, 1.0 mg progesterone; Group 2, 0.1 mg estradiol-17 beta; Group 3, 1.5 mg corticosterone, all at 6 h prior to expected ovulation; Group 4, 1.0 mg testosterone at both 8 h and 5 h before expected ovulation; and Group 5, 25 micrograms of ovine luteinizing hormone (LH) at 8 and 50 micrograms ovine LH at 6 h before expected ovulation. For each group, 4 control hens were injected with AG and the appropriate vehicle. Blood samples were taken at 1- or 2-h intervals from the time of AG injection to the expected time of ovulation. The hens were killed 4 h after expected ovulation and examined for the occurrence of ovulation. In all hens injected with vehicle, ovulation and the preovulatory surges of progesterone, testosterone, estradiol-17 beta and LH were inhibited. The plasma concentration of corticosterone was not reduced following an injection of AG. Four of 6 hens ovulated in response to injection of ovine LH, although neither endogenous LH nor progesterone were released. Thus, LH appears to play a direct role in follicular rupture and extrusion of the ovum. The administration of progesterone induced a significant and prolonged rise in LH, restoring AG-blocked ovulation in all hens treated (n = 6). Injections of testosterone restored LH release in all hens and ovulation in 2 of 7 hens treated. Three of 7 hens ovulated in response to the corticosterone injection. A preovulatory rise in LH was not observed, indicating that corticosterone may exert its ovulation-inducing effect directly on the mature follicle. Estradiol-17 beta did not restore LH release or ovulation in any of the hens treated with AG.

Aminoglutethimide↗
PubMed1984

Effects of pentobarbital anesthesia on tonic luteinizing hormone secretion in the ewe: evidence for active inhibition of luteinizing hormone in anestrus.

In the ewe, seasonal anestrus appears to result from two effects of inhibitory photoperiod: 1) estradiol gains the capacity to suppress luteinizing hormone (LH) pulse frequency and hence becomes a potent inhibitor of tonic LH secretion and 2) a steroid-independent decrease in LH pulse frequency occurs in ovariectomized ewes. In this study, we have obtained evidence, using pentobarbital anesthesia, that both these actions of photoperiod reflect the activation, in anestrus, of an inhibitory neural system. Administration of pentobarbital to intact anestrous ewes produced a dramatic, 3-fold increase in LH pulse frequency during the 6 h of anesthesia. In contrast, during the breeding season, pentobarbital inhibited LH pulse frequency in luteal phase animals. There was also a seasonal variation in the effects of pentobarbital in ovariectomized ewes. During the breeding season this drug again suppressed LH secretion, inhibiting both LH pulse amplitude and frequency. In anestrus, pentobarbital also suppressed pulse amplitude, but it produced a transitory increase (lasting 3 h) in pulse frequency. To account for the stimulatory actions of pentobarbital, we propose that in anestrus, but not the breeding season, LH pulse frequency is held in check by a set of estradiol-sensitive inhibitory neurons. Further, we suggest that these neurons are activated by inhibitory photoperiod and account for both the steroid-dependent and steroid-independent actions of photoperiod.

Anesthesia↗