Increase In Luteinizing Hormone Levels Research Articles

Sexual differentiation of the luteinizing hormone response of neonatal rats to the narcotic antagonist naloxone: critical role of estrogen receptors.

Administration of the narcotic antagonist naloxone results in an elevation of serum luteinizing hormone (LH) levels in 10-day-old female, but not male, rats. Previous studies from this laboratory indicated a role for neonatal gonadal steroids in the development of this sex-specific response. In this study, the estrogen receptor antagonist OH-Tamoxifen or the androgen-receptor antagonist flutamide were injected on Days 1 or 9 of life, and the LH responses of male and female pups to naloxone were assessed on Day 10. Flutamide did not produce a response different from that seen in vehicle-treated pups, discounting a role for androgen receptors. OH-Tamoxifen on Day 9 caused an increase in basal levels of LH; neither sex showed a response to naloxone. However, OH-Tamoxifen treatment of 1-day-old males resulted in an enhanced release of LH upon challenge with naloxone on Day 10 of life; similar treatment of 1-day-old females resulted in a normal female-type response to the opioid antagonist. These results show that blockade of estrogen receptors in males during the "critical period" of sexual differentiation results in a female phenotypic response to naloxone. Therefore, estrogen receptors play a critical role in the sexual differentiation of the LH response to naloxone in neonatal male rats.

Effect of exposure to the altitude of 300 meters below sea-level on testosterone, luteinizing hormone, follicle-stimulating hormone and prolactin in man.

Serum testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) responses to exposure to sea-level altitude (LA) were examined in 13 eugonadal males, age 21-22 yr, 3 and 5 days after residing at LA and on the second day of return to basal altitude 90 days later. After 3 days at their respective residence altitude, there was elevation in LH (p less than 0.05) and depression in testosterone levels (p less than 0.05), with similar results on day 5. These effects were all of transient nature, LH and testosterone concentrations returned to their basal levels on second day of the return to basal altitude. The FSH and PRL levels did not show any significant change during the stay at LA or after return to basal altitude. The observations suggest that exposure to LA is associated with increase in plasma levels of LH and decrease in testosterone. The decreased levels of testosterone could be due to a reduction in the sensitivity of the testis to LH, or due to inhibition of steroidogenesis in the testis.

Characterization and possible opioid modulation of N-methyl-D-aspartic acid induced increases in serum luteinizing hormone levels in the developing male rat

It has been previously reported that the excitatory amino acid, N-methyl-D-aspartic acid (NMDA), elicits prompt increases in serum luteinizing hormone (LH) levels in young male rats. The present studies were carried out to determine whether the effects of NMDA on LH were mediated by the release of LHRH from the hypothalamus. We also examined whether NMDA-sensitive neuronal pathways interacted with the endogenous opioid system regulating LHRH release and the ontogeny of NMDA-evoked increases in serum LH. We found that the age-response curve for NMDA-induced increases in LH was an inverted U; at early ages (10 and 15 days) the amino acid was marginally effective in increasing LH levels, it became maximally effective from post-natal days 20–40 and thereafter rapidly lost its efficacy such that it was virtually inactive in adult animals. Dose-response curves revealed that adult animals were more than 10-fold less sensitive to NMDA than their younger counterparts. Our studies also demonstrated that NMDA increased LH via a direct effect on the hypothalamic release of LHRH since a potent LHRH antagonist competitively inhibited the effects of NMDA. Finally, we observed that morphine competitively inhibited the effects of NMDA on LH release, suggesting a relationship between NMDA-sensitive neuronal pathways and those endogenous opioid-containing systems which are known to regulate LH release.

The usefulness of corticoids in stimulated cycles for in vitro fertilization.

1 Editorials in this journal do not necessarily reflect either the Editorial Board's or the publisher's opinion. z To whom correspondence should be addressed at Institute of Reproductive Endocrinology and in Vitro Fertilization, Trauttmansdorffgasse 3A, 1130 Vienna, Austria. spective randomized crossover trial that the combination of dexamethasone and clomiphene citrate produced significantly more pregnancies than clomiphene citrate alone when given to anovulatory or oligomenorrhoeic women. In these women DHEAS estimations were performed before the treatment and it could be seen that the improved ovulation and pregnancy rate with dexamethasone was restricted to those patients who had DHEA-S levels above 200 ixl/dl and was not seen in patients with DHEA-S levels below 200 ixl/dl. This supported the concept that the mechanism of action of dexamethasone was through adrenal suppression. In fact, there were reports that adrenal suppression with corticoids was explicitly successful in patients with hyperandrogenism (7) and with polycystic ovarian syndrome (PCO) (5). In 1970, Yen et al. (8) explained for the first time the ovulatory failure in PCO by an increased luteinizing hormone (LH) output of the pituitary gland which was the result of a positive feedback action caused by estrogens originating peripherally by conversion from adrenal androgens. In addition, Daly et al. proposed a direct detrimental effect of adrenal androgens on ovarian follicles (6). So far, adrenal suppression with corticoids seems indicated primarily in patients with signs of adrenal hyperandrogenism. However, most of the patients recruited for in vitro fertilization (IVF) do not have signs of hyperandrogenism, nor do they have cycle abnormalities. But many of them develop increased LH levels under stimulation therapy (9,10). This could be the result of the same mechanism which Yen et al. have described, except that the functional disturbance arises in a relatively shorter period of time. It is easily conceivable that any treatment for infertility--especially an IVF t reatment--can cause considerable stress for the patients, which may be the reason for an increased adrenal androgen output. In order to study the effect of adrenal suppression by corticoids on the results of IVF, we started a pilot study in 1984 whereby every treatment cycle for IVF was supplemented with prednisolone, 7.5

Gonadotropin-releasing hormone (GnRH) receptor dynamics and gonadotrope responsiveness during and after continuous GnRH stimulation.

Gonadotrope responsiveness, serum and tissue levels of luteinizing hormone (LH), and tissue concentration of gonadotropin-releasing hormone (GnRH) receptors in ovariectomized rats were determined during and after continuous GnRH stimulation. Intraperitoneal placement of GnRH-containing osmotic minipumps for 96 h established a rate of GnRH delivery (1 microgram/h) that resulted in stable serum levels of GnRH (500-700 pg/ml). Secretion of LH increased 8-fold within 6 h; however, serum LH returned to pretreatment levels by 24 h, even with continued GnRH stimulation. Tissue concentration of LH was depressed within 48 h of initiation of treatment but levels were restored by 96 h. Tissue levels of GnRH receptor remained elevated during the first 6 h of treatment but were reduced by 60% within 24 h and remained depressed for the duration of treatment. Gonadotrope responsiveness 48 h and 96 h after initiation of treatment was reduced by 50% and 90%, respectively. Removal of the GnRH delivery vehicle resulted in rapid disappearance of GnRH from serum. Dramatic reduction (75%) in circulating levels of LH, and a 2-fold increase in tissue levels of LH and in GnRH receptor concentration were noted within 6 h of minipump removal. Although tissue concentration of GnRH receptor returned to pretreatment levels within 48 h of minipump removal, both basal LH secretion and gonadotrope responsiveness remained depressed even 96 h after cessation of continuous GnRH stimulation. These data indicate that GnRH can "down regulate" its receptor, gonadotrope responsiveness is not obligatorily linked to receptor concentration, and desensitization that follows hyperstimulation represents effects directed at post-receptor loci.

Changes in Circulating Levels of Immunoreactive Follicle Stimulating Hormone, Luteinizing Hormone, and Testosterone During Sexual Development in the Rhesus Monkey, Macaca mulatta

Basal serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone (T) and the responsiveness of these hormones to a challenge dose of luteinizing hormone releasing hormone (LHRH), were determined in juvenile, pubertal, and adult rhesus monkeys. The monkey gonadotrophins were analyzed using RIA reagents supplied by the World Health Organization (WHO) Special Programme of Human Reproduction. The FSH levels which were near the assay sensitivity in immature monkeys (2.4 +/- 0.8 ng/ml) showed a discernible increase in pubertal animals (6.4 +/- 1.8 ng/ml). Compared to other two age groups, the serum FSH concentration was markedly higher (16.1 +/- 1.8 ng/ml) in adults. Serum LH levels were below the detectable limits of the assay in juvenile monkeys but rose to 16.2 +/- 3.1 ng/ml in pubertal animals. When compared to pubertal animals, a two-fold increase in LH levels paralleled changes in serum LH during the three developmental stages. Response of serum gonadotrophins and T levels to a challenge dose of LHRH (2.5 micrograms; i.v.) was variable in the different age groups. The present data suggest: an asynchronous rise of FSH and LH during the pubertal period and a temporal correlation between the testicular size and FSH concentrations; the challenge dose of LHRH, which induces a significant rise in serum LH and T levels, fails to elicit an FSH response in all the three age groups; and the pubertal as compared to adult monkeys release significantly larger quantities of LH in response to exogenous LHRH.

Central, stereoselective receptors mediate the acute effects of opiate antagonists on luteinizing hormone secretion

Although a central site of acute opiate action in regulating luteinizing hormone (LH) secretion has been suggested by the ability of centrally implanted opiate antagonists to increase LH levels, opiate antagonists are lipophilic and could influence the pituitary in situ . Also, the physiological significance of opiate receptor blockade with antagonists rests on the assumed, but untested, stereoselectivity of these receptors. Therefore, a lipophobic quanternized derivative of naltrexone (MRZ 2663-Naltrexone methobromide) and dextro- (+) and levo- (−) stereoisomers of naloxone were used to study the site- and stereoselectivity of gonadotropin responses to opiate antagnoists in vivo . Male rats were injected intracerebroventricularly (icv) or intravenously (iv) with the quarternary or tertiary congeners of naltrexone and subcutaneously (sc) with (−) or (+)-naloxone. Rats injected icv with 20 ug of quaternary naltrexone displayed significant increases in serum luteinizing hormone (LH). The onset of the response was rapid with serum LH levels being significantly elevated 15 minutes after the injection and returning to basal levels 30 minutes later. Rats injected iv with 10 mg/kg of quaternary naltrexone failed to show significant LH responses. Rats injected either centrally or periphally with equivalent doses of tertiary naltrexone showed LH responses that were similar to those found in animals injected icv with quaternary naltrexone. As little as 0.5 mg/kg of (−)-naloxone resulted in significant elevations in serum LH that were higher than those elicited by up to 10 mg/kg of (+)-naloxone, indicating that this effect of naloxone is stereoselective. These data support the argument that opioids can acutely modulate LH secretion through actions at stereoselective opioid receptors in the central nervous system.

Opioid regulation of luteinizing hormone secretion in the male rat.

Current evidence suggests that endogenous opioid peptides (EOPs) tonically inhibit secretion of luteinizing hormone (LH) by modulating the release of gonadotropin-releasing hormone (GnRH). Because of their apparent inhibitory actions, EOPs have been assumed to alter both pulse frequency and amplitude of LH in the rat; and it has been hypothesized that EOP pathways mediate the negative feedback actions of steroids on secretion of GnRH. In order to better delineate the role of EOPs in regulating secretion of LH in the male rat, we assessed the effects of a sustained blockade of opiate receptors by naloxone on pulsatile LH release in four groups: intact male rats, acutely castrated male rats implanted for 20 h with a 30-mm capsule made from Silastic and filled with testosterone, acutely castrated male rats implanted for 20 h with an osmotic minipump dispensing 10 mg morphine/24 h, and male rats castrated approximately 20 h before treatment with naloxone. We hypothesized that if EOPs tonically inhibited pulsatile LH secretion, a sustained blockade of opiate receptors should result in a sustained increase in LH release. We found that treatment with naloxone resulted in an immediate but transient increase in LH levels in intact males compared to controls treated with saline. Even though mean levels of LH increased from 0.15 +/- 0.04 to a high of 0.57 +/- 0.14 ng/ml, no significant difference was observed between the groups in either frequency or amplitude of LH pulses across the 4-h treatment period. The transient increase in LH did result in a 3- to 4-fold elevation in levels of plasma testosterone over baseline. This increase in testosterone appeared to correspond with the waning of the LH response to naloxone. The LH response to naloxone was eliminated in acutely castrated rats implanted with testosterone. Likewise, acutely castrated rats treated with morphine also failed to respond to naloxone with an increase in LH. These observations suggest that chronic morphine and chronic testosterone may act through the same mechanism to modulate secretion of LH, or once shut down, the GnRH pulse-generating system becomes refractory to stimulation by naloxone. In acutely castrated male rats, levels of LH were significantly increased above baseline throughout the period of naloxone treatment; this finding supports the hypothesis that the acute elevation in testosterone acting through mechanism independent of opioid is responsible for the transient response of LH to naloxone in the intact rat.

Seasonal Changes in Plasma Levels of LH and Gonadal Steroids in Free-Living Willow Tits Parus montanus

Seasonal variations in plasma levels of luteinizing hormone (LH), dihydrotestosterone (DHT), testosterone and estradiol (only in females) were studied in free-living adult and juvenile Willow Tits from southwest Sweden. All hormones, except DHT, showed pronounced annual cycles. For both sexes, and both age groups, LH titers showed a typical bimodal pattern with transitional peaks during the breeding period and early autumn. Also, LH levels increased significantly in January and remained elevated throughout the winter. Male plasma levels of testosterone also showed a bimodal pattern with peaks occurring concomitant with LH. The August September peak was, however, caused by some juveniles having very high plasma levels of testosterone, whereas the majority of juveniles and all adults showed low testosterone levels at this time. Female testosterone values did not vary significantly during the year, but in junvenile females testosterone levels showed a transitional peak in August. Estradiol showed only one significant annual peak during the breeding period. The winter increase in plasma levels of LH was not accompanied by changes in testosterone, or estradiol, titers. In spring, male LH and testosterone levels started increasing a month earlier than LH and estradiol in females.

Ontogeny of secretory patterns of LH release and effects of gonadectomy in the chronically catheterized pig fetus and neonate.

Two experiments were conducted to determine the ontogeny of secretory patterns of luteinizing hormone (LH) release and effects of gonadectomy on the characteristics of LH secretion in the chronically catheterized pig fetus and neonate. To study secretory patterns in intact animals, blood samples were collected from 44 pig fetuses and their mothers (Days 81, 99, 109 and 113 of gestation) as well as from 25 neonates (Days 4 and 8) every 15 min for 3 h (2 h on Day 81). The results indicate that the fetal adenohypophysis secretes occasional pulses of LH as early as Day 81 of fetal life. Fetal and maternal mean LH levels are low (0.25-0.50 ng/ml) at all gestational ages, with lowest values just before birth (Day 113 post coitum). Four-day-old neonates show a significant increase in pulse frequency (male and female) as well as pulse amplitude (female), relative to fetal values, leading to significant augmentations in mean LH levels. This is associated with reductions in both 17 beta-estradiol and progesterone. By 8 days of age significant sex differences in mean LH levels (males greater than females) appear. Testosterone/5 alpha-dihydrotestosterone levels (males) are low prenatally but are significantly increased after birth, possibly due to the stimulating effects of increasing LH levels. To study the gonadal control of LH secretion, forty-one 105-day-old fetuses and thirty-eight 4-day-old neonates were chronically catheterized and were either gonadectomized or remained as sham or control animals. Forty-eight and 96 h after surgery, blood samples were taken every 15 min for 3 h. No significant changes are detectable at 96 h in mean LH, pulse frequency and amplitude in female or male fetuses or in neonates. While significant reductions in testosterone levels are observed at 96 h in the male fetus and neonate, progesterone concentration is reduced only in the neonate. In the castrated female, on the other hand, neither fetus nor neonate display significant changes in circulating levels of progesterone and 17 beta-estradiol at 96 h. It is concluded that the pituitary of the pig is able to discharge LH with occasional pulses as early as Day 81 of fetal life; however, the pituitary remains suppressed until after birth, probably due to high circulating nongonadal steroids in the fetal compartment.

Changes in LH and prolactin levels in diabetic male rats and the role of the opiate system in the control of their secretion

Diabetic male rat has low serum levels of luteinizing hormone (LH) and testosterone (T), which are accompanied by atrophy of the testes and accessory glands. The present study investigated changes in the serum levels of LH, prolactin (PRL) and glucose, following diabetes induction by streptozotocin. In addition, involvement of the opiate system in the control of LH and PRL secretion was evaluated. There was no difference in PRL levels between diabetic and control animals, except at 8 hours after streptozotocin injection. In contrast, the diabetic animals had consistently lower levels of LH, starting on the second day of diabetes. Blockade of the opiate system by naltrexone caused a sharp increase of LH levels in normoglycemic rats, while only a gradual decrease was observed in hyperglycemic animals. PRL secretion was inhibited by naltrexone, both in diabetic and control groups. It is concluded that, unlike normoglycemic rats, inhibition of LH secretion in diabetes is not under the control of the opiate system, probably as a result of T deficiency. In contrast, PRL secretion in diabetic rats, as in the control group, is under the influence of endogenous opiates.

Investigation of sex hormones in male epileptic patients.

Testosterone (T), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin (PRL) levels were obtained in 33 male epileptic patients and 11 age-matched normal controls. The patients had significantly higher mean levels of FSH, LH, and PRL; T was decreased but not significantly so. Patients who had reported difficulties with sexual arousal on the Bear-Fedio Inventory had significantly lower T levels than those who did not. Increased LH levels correlated with younger age at onset of epilepsy and longer history of tonic clonic seizures. Increased PRL levels were related to a positive family history of epilepsy and nonfocal tonic clonic seizures. Anticonvulsant levels were unrelated to hormonal changes except for carbamazepine which was positively correlated with PRL levels.

Role of the septum on LH, FSH and prolactin secretion in male rats

Serum concentrations of luteinizing hormone (LH) follicle-stimulating hormone (FSH), prolactin (PRL) and testosterone were measured by radioimmunoassay in male Wistar rats: 1. (a) Four days after a septal lesion ( n = 19) and 2. (b) Just following electrical stimulation of the septum ( n = 15). Septal lesions induced a significant decrease in serum LH (16.37 ± 2.01 vs. 30.27 ± 2.08 ng/ ml; p < 0.001) and testosterone concentrations (0.53 ± 0.05 vs. 1.01 ± 0.14 ng/ ml; p < 0.02). No significant changes were observed for FSH or PRL levels. Electrical septal stimulation induced an increase in serum levels of LH (211.5 ± 46.4 vs. 29.6 ± 11.5 ng/ ml; p < 0.01) and FSH (703 ± 83 vs. 378 ± 57 ng/ ml; p < 0.01), without changes in PRL or testosterone concentrations. From these data we conclude that in male rats the septum may play a role in the mechanisms controlling gonadotropins release by the anterior pituitary gland.

Phase II evaluation of Lonidamine in patients with advanced malignancy.

Lonidamine, a substituted indazole carboxylic acid with unique effects on cellular respiration, was studied in 27 patients with advanced malignancies. Of the 18 evaluable patients, 5 had small-cell lung cancer, 3 had non-small-cell lung cancer, 3 sarcoma, 2 breast cancer, and 5 other tumour types. All but 1 had had extensive prior treatment. A partial response was seen in 1 patient with metastatic synovial sarcoma, and tumour growth inhibition was demonstrated in 2 other cases. The major toxicity encountered was myalgia (66.6%) which was incompletely ameliorated by prednisone and required dose reduction in 2 patients and cessation of drug in 3. Other toxicities included auditory changes, anorexia, nausea and vomiting, diarrhoea, skin sensitivity, and conjunctivitis. No added toxicity was seen, when Lonidamine was combined with other chemotherapeutic agents. No correlation between Lonidamine dose and serum lactate levels was seen, although 4 patients showed a progressive increase in lactate levels over time, thought to be related to their increasing tumour burden. 5 patients demonstrated a dramatic fall in serum testosterone levels 4-8 weeks after starting Lonidamine which was accompanied by an increase in luteinizing hormone levels in 3 patients. In summary, modest antitumour activity was demonstrated in 3 patients; moderate toxicity was seen in most patients, but was usually tolerable. Further studies of Lonidamine are warranted in less heavily treated patients, alone or in combination with other chemotherapeutic agents.

Effects of estrogen and progesterone on serum prolactin and luteinizing hormone levels in ovariectomized turkeys ( Meleagris gallopavo)

Serum prolactin (PRL) and luteinizing hormone (LH) levels from mature female turkeys were determined following ovariectomy and daily subcutaneous injections for 4 or 9 days of 0.002–2.0 mg/kg estradiol benzoate (EB), 0.05–2.0 mg/kg progesterone (P), or their combinations. Serum PRL levels were increased ( P < 0.05) at the onset of sexual maturity in intact controls, but not in ovariectomized turkeys. Injection of 0.02 mg/kg EB into ovariectomized turkeys resulted in elevated ( P < 0.05) serum PRL levels after 8 treatment days. Higher doses failed to elicit a response of greater magnitude. EB at doses of 0.02–2.0 mg/kg reduced LH levels while 0.002 mg/kg EB increased LH levels above ( P < 0.05) those of ovariectomized controls. The 1.0-mg/kg P dose increased ( P < 0.05) serum PRL within 24–48 hr of administration while the 0.05-, 0.5-, or 2.0-mg/kg P doses failed to elicit a response. When P was injected in doses of 0.5–2.0 mg/kg, LH levels were decreased in a dose-response manner. The injection of EB combined with P had a variable effect on serum PRL levels. The 0.5- or 1.0-mg/kg dose of P facilitated (advanced in time) the rise in serum PRL level induced by 0.02 mg/kg of EB. In contrast, the positive feedback effect of 0.2 mg/kg of EB was blocked when administered with 0.5 mg/kg of P. Serum LH levels were dramatically decreased by all steroid combinations used. These results indicate that daily injections of EB and/or P in ovariectomized turkeys have a variable effect on serum PRL and LH levels depending upon the dose, the duration of treatment, or the ratio between EB and P.

Importance of retinal photoreceptors to the photoperiodic control of seasonal breeding in the ewe.

Two experiments were performed to determine whether the eyes are necessary for photoperiodic control of reproduction in ewes. In the first, intact and estradiol-treated ovariectomized (OVX + E) ewes were housed in each of 2 photoperiod-controlled rooms with a vasectomized ram and subjected to 90-day alternations between long and short days. Prior to blinding, long days initiated anestrus in intact ewes and a suppression of serum luteinizing hormone (LH) levels in OVX + E ewes; short days caused onset of estrous cycles and an increase in LH levels in the intact and OVX + E ewes, respectively. After 1.5 years of such photoperiodic control, all ewes were blinded by bilateral orbital enucleation. Photoperiodic control was lost following blinding, but circannual alternations between cyclicity and anestrus or high and low LH levels, were maintained in most ewes for the remaining 2.5 years of the study. In one group of OVX + E ewes, serum LH levels remained synchronized to the 90-day shifts in photoperiod for about 1 year after blinding. Once the sighted ram was removed from the room, however, the 90-day rhythm in LH disappeared and a circannual pattern of LH became evident, suggesting that blind ewes may receive photoperiodic information from a sighted ram. This possibility was supported by the results of the second experiment in which 12 additional OVX + E ewes were blinded and exposed to 90 long days and 90 short days in the absence of a sighted ram. In these ewes, serum LH levels were not controlled by the changes in photoperiod. These results are consistent with the following conclusions: 1) the eyes are necessary for perception of photoperiod in the ewe and 2) ewes have an endogenous circannual rhythm of reproduction and/or they can be controlled by other environmental signals in the absence of photoperiodic input. Further, the results lead to the hypothesis that blind ewes can receive photoperiodic information indirectly from a sighted ram.

Seasonal Variations in the Ultrastructure of the Leydig Cells and Plasma Levels of Luteinizing Hormone and Steroid Hormones in Juvenile and Adult Male Great Tits Parus major

Annual cycles in plasma levels of luteinizing hormone (LH), testosterone and dihydrotestosterone (DHT), as well as seasonal changes in the ultrastructure of Leydig cells, were studies in free-living adult and juvenile male Great Tits from south-west Sweden. Special attention was paid to the autumn/winter period. Adult males have very few Leydig cells during the autumn, whereas such cells occur in large numbers in the testes of juvenile Great Tits. At the end of the autumn period there is an increase in plasma levels of LH, but not in testosterone, in both age groups. This increase is accompanied by changes in number and ultrastructure of the Leydig cells, especially in adults, so that there is finally no longer any differences between adults and juveniles. For both age groups the ultrastructure of the Leydig cells indicate maximal activity during the winter period, but testosterone levels remain basal. There are no differences in plasma levels of testosterone or LH between juvenile and adult males during the autumn/winter period, except during September when the plasma concentrations of these hormones are significantly higher in juveniles. There is a transitory increase, to maximal values for the year, in plasma levels of LH and testosterone in March. Concomitant with this increase the ultrastructure of the Leydig cells change. The breeding period is characterized by moderate plasma levels of testosterone and LH. There is a trend for higher levels of LH, but not for testosterone, in June. Plasma levels of both hormones are down to basal in July. When testes regress in July, most Leydig cells are in a state of dissolution. Plasma levels of DHT did not show an annual cycle. Ecological and behavioural implications of the results are discussed.

Serum gonadotrophins in Down's syndrome.

Serum levels of follicle stimulating hormone (FSH) and luteinising hormone (LH) in institutionalised male patients with Down's syndrome (DS) have been found to be significantly higher than in age matched controls from the same institution. This difference is found in patients both under and over 30 years of age with respect to FSH levels, but the increase in LH levels is confined to patients with DS over 30.

Ontogeny of sex differences in LH and FSH levels 48 h after castration in the rat.

Serum gonadotropin levels were measured 12, 24, and 48 h after gonadectomy in male and female rats (ages, 22--60 days) to assess when during development the rate of rise of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) after castration approximates that seen in the gonadectomized adult. In females serum LH levels 48 h after ovariectomy were increased above sham levels only when the ovaries were removed prior to vaginal opening. Ovariectomy on the day of vaginal opening or at older ages resulted in no increase in LH levels by 48 h after surgery. Serum FSH levels at 24 and 48 h after ovariectomy declined with increasing age at the time of ovariectomy. In males serum LH levels at 48 h after castration increased with increasing age at the time of gonadectomy. Serum FSH levels at either 12, 24, or 48 h after orchidectomy did not change appreciably with age at the time of surgery. It is concluded that the acute pituitary secretion of gonadotropins after removal of testes in the immature male resembles that seen in the mature male early in the course of the development of sexual maturity. In contrast, the acute pituitary secretion of gonadotropins after removal of the ovaries in the immature female does not resemble that seen in the ovariectomized adult until she is mature and capable of ovulating. Thus, the observed delay in the rise of LH seen in ovariectomized adults may be a function of some aspect of the hormonal changes associated with the estrous cycle.

Temporal relationship between progestin and luteinizing hormone concentrations in pseudopregant rats treated with prostaglandin-F 2α

The temporal changes in progesterone (Δ 4P), 20α-dihydroprogesterone (20α-DHP) and luteinizing hormone (LH) concentrations in pseudopregnant (PSP) rats after treatment with a single subcutaneous Silastic-PUP tube containing 600 μg PGF 2α were correlated. Progesterone levels fell and LH levels rose significantly 2h after initiation of treatment, while 20α-DHP levels were fond to increase significantly 12h after treatment. Since the changes in Δ P and LH concentrations occurred concurrently, it seems that the increase in LH levels could have been due to a direct effect of PGF2a on the ovary causing a reduction in Δ 4P and thus a negative feedback effect on LH release. Alternatively, PGF2a might exert a direct effect on LH secretion at the hypothalamic-pituitary level.