Rise In Plasma Luteinizing Hormone Research Articles

Female pheromones stimulate release of luteinizing hormone and testosterone without altering GnRH mRNA in adult male Syrian hamsters ( Mesocricetus auratus)

In many species chemosensory stimuli function as important signals that influence reproductive status. Neurons synthesizing the peptide gonadotropin-releasing hormone (GnRH) are critical mediators of reproductive function via their regulation of the hypothalamic–pituitary–gonadal (HPG) axis, and they are thought to be responsive to chemosensory information. In the present study, we sought to elucidate the effects of female chemosensory stimuli on the HPG axis in sexually naive adult male Syrian hamsters. In Experiment 1, serial blood samples were collected from catheterized male hamsters following exposure to female pheromones in order to characterize the luteinizing hormone (LH) response to this chemosensory stimulus. In Experiment 2, brains and terminal blood samples were collected from animals 0, 60, and 120 min following pheromone exposure. GnRH mRNA was measured in brain tissue sections using in situ hybridization, and plasma concentrations of LH and testosterone were measured using radioimmunoassay. Data from Experiment 1 indicated that female pheromones elicited a rapid rise in plasma LH that peaked at 15 min and returned to baseline 45 min after exposure. In Experiment 2, testosterone was elevated in terminal blood samples obtained 60 min, but not 120 min, after exposure to pheromones. LH levels were unaffected at both of these time points. The chemosensory-induced increases in LH and testosterone release were not accompanied by subsequent changes in GnRH mRNA over the time course studied. These data suggest that while activation of the male HPG axis by female pheromones involves release of GnRH, it does not involve increases in GnRH mRNA 1–2 h after pheromonal stimulation as a mechanism for replenishment of released peptide.

The Peripheral Levels of Luteinizing Hormone(LH), Follicle-Stimulating Hormone(FSH), Immunoreactive(ir-) Inhibin, Progesterone(P) and Estradiol-17.BETA.(E2) at the Time of Control of Ovulation With Gonadotropin Releasing Hormone(GnRH) Agonist(Deslorelin) in Pony Mares.

Control of ovulation in mares obviously has many advantages in a breeding program. Two pony mares were challenged against synthetic Gonadotropin Releasing Hormone (GnRH) agonist (Deslorelin) for six consecutive cycles. Clinical and endocrinological findings after treatment (n=6) with GnRH agonist were compared with those of the control findings before treatment (n=3) of the same mares. The time interval from administration of the GnRH agonist till ovulation (43.5 ± 4.0 hr) and the length of the estrous cycle (19.5 ± 1.0 days) at the time of treatment were significantly (p<0.05) shortened as compared with those of the control. A preovulatory sharp rise in plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) was also noticed 24 hr from the time of GnRH agonist injection and one day prior to ovulation in the studied mares, but there were no significant differences before and after treatment with GnRH agonist on the levels of ir-inhibin, progesterone (P) and estradiol-17 β (E2). It seems likely that GnRH agonist is beneficent in reducing the number of matings needed for conception in a natural mating program and that ovulation in mares may be induced by a sharp preovulatory rise in LH and FSH.

Reproduction: Effect of GNRH and HCG administration on plasma LH and testosterone concentrations in normal stallions, aged stallions and stallions with lack of libido

Summary Gonadotrophin‐releasing hormone (GnRH) (a single intravenous injection with 0.042 mg busereline acetate) was administered to control stallions (n=5), aged stallions (n=5) and stallions with lack of libido (n=5). Jugular blood samples were taken at ‐10, 0, 10, 20, 40 and 80 minutes after treatment and measured for luteinizing hormone (LH) and testosterone concentrations. A single intravenous injection of hCG (3000 IE) was given 1 day later. Venous blood samples were taken at ‐60, 0, 15, 30, 60, 120, and 240 minutes after treatment and measured for the testosterone concentration. The experiment was performed in the breeding season. There was a wide variation between stallions in basal concentrations of LH and testosterone. The treatment groups all showed a significant increase in LH and testosterone concentrations after treatment with GnRH. There was a significant difference (P<0.05) between the control, the lack of libido stallions and the aged stallions in the production of LH before and after stimulation with GnRH. The aged stallions had higher basal LH concentrations. GnRH induced a rise in plasma LH in all groups, but the greatest response was observed in aged stallions. No response to GnRH was seen with respect to plasma testosterone. There was an increase in plasma testosterone following hCG; however, this increase was very small in aged stallions. After stimulation with hCG the control and lack of libido stallions had a significant increase (P<0.05) in testosterone production. In conclusion, stimulation with either GnRH or hCG can be a valuable method to test whether the function of the stallion's reproductive endocrine system is optimal.

Isolation and partial characterization of tammar wallaby luteinizing hormone and development of a radioimmunoassay.

Tammar wallaby (Macropus eugenii) luteinizing hormone (LH) was purified from pituitaries collected from wild and captive populations by salt sequential precipitation, ion exchange chromatography and gel filtration. Pituitary tissue (5 g) yielded 1.8 mg of purified wallaby luteinizing hormone (ME-14B), as verified by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). A heterologous radioimmunoassay has been developed for measurement of LH in plasma of marsupials using a monoclonal antibody raised against bovine LH (518B7). This assay system was able to measure basal LH concentrations in male and female tammars and detected a significant rise in plasma LH in response to oestradiol benzoate in female tammars and luteinizing hormone-releasing hormone (LHRH) in males. Parallel dose-response curves were also obtained from pituitary extracts from four other species of marsupial (brushtail possum, Trichosurus vulpecula; brown antechinus, Antechinus stuartii; kowari, Dasyuroides byrnei; and Eastern pygmy possum, Cercartetus nanus) in this assay, which suggests its usefulness in the measurement of LH in other marsupial species.

The photoperiodic clock in blackheaded buntings (Emberiza melanocephala) is mediated by a self-sustaining circadian system

Three experimental protocols were employed to clarify whether the circadian system is involved in photoperiodic time-measurement in the blackheaded bunting, Emberiza melanocephala. In a single-pulse paradigm, one 8-h light pulse was delivered at different times to groups of birds across three days of constant darkness (DD). Photoperiodic induction, as measured by a rise in plasma luteinizing hormone (LH), showed clear circadian rhythmicity. The second experiment examined the LH responses in birds exposed to lighting cycles using a Nanda-Hamner type of protocol and confirmed full photostimulation under 6L:30D. The third experiment measured the time of the first photoinduced rise in LH in birds subjected to 30 h of continuous light following entrainment under short days (6L:18D). This experiment aimed to identify the position of the photoinducible phase (phi i). LH first rose at hour 18 following dawn indicating that phi i lies in the middle of the day. Plasma concentrations of melatonin were also measured under 6L:18D and 6L:30D light cycles as another physiological marker of the circadian systems in buntings. The pattern of melatonin secretion with the driving oscillator being circadian in nature. It is concluded that the circadian pacemaker driving the photoinducible rhythm in blackheaded bunting is strongly self-sustaining and free-runs under constant conditions.

Plasma levels of luteinizing hormone in intact and castrated photosensitive blackheaded buntings (Emberiza melanocephala) exposed to stimulatory and nonstimulatory photoperiods.

Experiments were performed to investigate the effects of castration and/or photostimulation on plasma luteinizing hormone (LH) in photosensitive blackhead buntings. Castration evoked a significant rise in plasma LH in birds held under 8 h light: 16 h darkness (8L:16D). On exposure to 18L:6D for 24 d, both the intact birds and the castrates exhibited a significant rise in plasma LH, although the change in LH levels in the castrates was approximately 8 times greater than in the intact birds. When control birds under 8L:16D which showed no change in plasma LH up to d 13 were transferred to a 36-h resonance cycle (8L:28D), plasma LH rose significantly within 4 cycles of the treatment. Furthermore, the intact buntings showed rapid increase and decrease in the plasma LH levels during a 16-wk exposure to long (16L:8D) but not to short (8L:16D) photoperiods. These results suggest that: i) the photoperiodic drive on LH secretion is inhibited by the testes; ii) the blackheaded bunting has a strong photoresponsive system; and iii) a circadian rhythm of photosensitivity is involved in the photoperiodic time measurement in this species.

Role of Gamma-Aminobutyric Acid in the Zona incerta in the Control of Luteinizing Hormone Release and Ovulation

gamma-Aminobutyric acid (GABA) neurones are present in the zona incerta (ZI) where other systems have been shown to influence gonadotrophin release. This report investigates the effect of GABA agents in the ZI on ovulation and luteinizing hormone (LH) release. In intact females under Saffan anaesthesia, bilateral stereotactic injections into the ZI of two GABA transaminase inhibitors [amino(oxy)acetic acid and gamma-acetylene GABA] on the morning of pro-estrus or two GABA agonists on the afternoon of pro-estrus inhibited ovulation. The selective GABA B agonist baclofen was effective at 0.05 nM; muscimol, a mixed GABA A and B agonist, was 50-fold less potent, while the selective GABA A agonist isoguvacine had no effect at 500 nM. Administration of baclofen at 0.05 and 5 nM into the ZI significantly reduced plasma LH concentration in untreated ovariectomized rats and also prevented the rise in LH normally induced in ovariectomised rats primed with 5 micrograms oestradiol benzoate (OB) plus 0.5 mg progesterone. In ovariectomised rats primed with 5 micrograms OB alone, administration of the selective GABA A antagonist bicuculline (200 and 260 pg/side) had no effect on plasma LH, while the GABA B antagonist phaclofen (10 pg/side) stimulated a rise in plasma LH, 40 and 60 min after injection. These results indicate that GABA activity in the ZI exerts an inhibitory effect on LH release and ovulation and this is preferentially exerted via GABA B receptors.

Effects of estrogen on hypothalamic gonadotropin-releasing hormone release in castrated male rhesus macaques

The evidence that hypothalamic gonadotropin-releasing hormone (GnRH) release increases during the estrogen-induced luteinizing hormone (LH) surge in castrated female macaques and that estrogen induces a similar LH surge in the male suggests that either sexual differentiation of GnRH secretion does not exist or that changes in brain GnRH are not critical for ovulation. We tested this hypothesis by using the push-pull perfusion (PPP) technique to monitor GnRH release in the mediobasal hypothalamus continuously from 10 h before to 50 h after estrogen injection in 9 castrated male rhesus macaques. Blood sampling and PPP were performed with monkeys freely moving in their own cage by using a specially designed swivel/tethering system. PPP samples were collected every 10 min and analyzed for GnRH concentration by radioimmunoassay. Blood samples were collected every hour and plasma LH was measured by bioassay. Estradiol benzoate (EB, 42 μg/kg, b. wt.) was subcutaneously injected after 10 h of initial PPP. The PPP was continued for 10 h after EB in 4 and 50 h after EB in 5 monkeys. Hypothalamic GnRH patterns were analyzed by the Pulsar algorithms. The results show that during the 10 h after EB, plasma LH declined rapidly, reaching low or non-detectable levels by 7–9 h, while hypothalamic GnRH releasing patterns did not change during this period ( n = 9). In contrast, estrogen enhanced GnRH level and pulse amplitude, but not pulse frequency, several hours before mean peripheral plasma LH increased from suppressed values ( n = 4). These data suggest that the immediate negative feedback effect of estrogen on LH release occurs mainly in the pituitary, and that estrogen subsequently stimulates hypothalamic release of GnRH in advance of the initial rise in plasma LH. The results further support the hypothesis that the gonadotropin-releasing mechanism in primates is functionally non-differentiated, and that increased release of hypothalamic GnRH is actively involved in regulating the estrogen-induced gonadotropin surge in both sexes.

Locus coeruleus (LC) stimulation augments LHRH release induced by medial preoptic stimulation. Evidence that the major LC stimulatory component enters contralaterally into the hypothalamus

Previous studies by others suggest that mid- and hindbrain noradrenergic projections to the hypothalamus may be stimulatory or inhibitory to luteinizing hormone releasing hormone (LHRH) release depending upon the steroid environment of the rat. In the present study we reevaluated the effects of electrical stimulation of the locus coeruleus (LC) in estrogen-primed ovariectomized (OVX) rats anesthetized with chloral hydrate. This anesthetic agent blocked the spontaneous luteinizing hormone (LH) surges which normally occur in estrogen-treated OVX rats. In such rats, bilateral LC electrical stimulation was ineffective in altering basal LH concentrations. Thereafter, we evaluated the effects of LC electrical stimulation on patterns and concentrations of plasma LH induced by electrochemical stimulation (ECS) of the medial preoptic nuclei (MPN). Bilateral MPN-ECS induced a significant rise in plasma LH. When the LC was bilaterally stimulated for 15 min beginning 30 min after MPN stimulation, peak LH concentrations were significantly augmented and remained elevated throughout the experiment. To learn more of how LC noradrenergic projections reach regions of the hypothalamus which contain LHRH neurons, the right MPN in a group of rats was unilaterally ECS and 30 min later the right LC was unilaterally stimulated for 15 min. Plasma LH levels increased after MPN activation but no further rise or fall in LH occurred after ipsilateral LC stimulation. In the final group of rats, the right MPN was unilaterally electrochemically stimulated and this was followed 30 min later by contralateral electrical stimulation of the left LC. In these animals, peak plasma LH concentrations were significantly elevated above those obtained after only unilateral MPN stimulation. These data demonstrated that LC stimulation augments LH release but only after preliminary depolarization of LHRH neurons by ECS. Moreover, the stimulatory noradrenergic projections from LC decussate to enter contralateral hypothalamic regions containing LHRH neurons.

Plasma reproductive hormones in normal and vasectomized Chinese males.

Plasma reproductive hormones (testosterone, LH, FSH and prolactin) were measured in 298 normal healthy males aged 30-73 years from rural areas of Sichuan Province, People's Republic of China, and in 505 similar men vasectomized between 1 year and 25 years previously. Age-related increases in LH and FSH but not in testosterone or prolactin were noted in normal men. No adverse effects of vasectomy were observed apart from a 16% increase in mean LH levels in the vasectomized compared to non-vasectomized men of similar ages.

Hormonal correlates of photoperiod-induced puberty in a reflex ovulator, the female ferret (Mustela furo).

In an attempt to develop an animal model wherein the pubertal process could be initiated or accelerated by a readily controlled, noninvasive, external signal, this study examined sexual development of the female ferret, a photoperiodic, reflex ovulator. These animals exhibit signs of precocious sexual maturation within 6 wk of exposure to a stimulatory, long-day photoperiod at 15 wk of age. In the first study, females matured under a long-day stimulus were allowed to mate with a fertile male ferret. All six females ovulated after mating, and three of six became pregnant and successfully delivered and reared litters, demonstrating that vulvar edema induced by long days reflected the onset of true precocious sexual maturation. The second study attempted to determine the endocrine basis of this photoperiod-induced puberty. Immature ferrets were either left intact or were ovariectomized at 13 wk of age. These females either remained untreated or immediately received an estradiol implant. Controls in each group remained in short days, and others were transferred to stimulatory long days at 16 wk of age. Results indicated that immature ferrets exhibited a rise in plasma luteinizing hormone (LH) upon ovariectomy, and that the extradiol implant was an effective negative feedback signal for the duration of the study in animals in short days. In contrast, females in long days exhibited an "escape" from LH inhibition by the steroid implant at the same age at which the intact females in long days were beginning to mature. These data suggest the young ferret exhibits a high sensitivity to estradiol negative feedback which is decreased in response to a stimulatory photoperiod, and which decrease is coincident with sexual maturation in intact animals under the same conditions.

Hypothalamic neurotransmitter function in experimentally induced hyperprolactinemia

It is known that animals or patients bearing a prolactin (PRL)-secreting tumor (PST) do not suppress PRL levels after administration of indirectly acting dopamine agonists, namely nomifensine (Nom), and are not responsive to the PRL releasing effect of antidopaminergic drugs and opioid peptides. Since the action of these drugs is mediated through the tuberoinfundibular dopaminergic (TIDA) system, these findings have been taken to indicate that animals and humans bearing prolactinomas have a defective TIDA function. Alternatively, PRL unresponsiveness to these drugs could be due to hyperfunction of TIDA system for the feedback action of high PRL levels. To clarify whether hypo- or hyperfunction of the TIDA system was responsible for such behaviour, we tested the effect of a synthetic opioid peptide (FK 33–824), a DA receptor antagonist, domperidone (Dom), and of Nom on PRL secretion in two experimental models of non-tumoral hyperprolactinemia, i.e. rats bearing ectopic pituitaries since 3 days (TP rats), or treated with ovine PRL (oPRL 250 μg, twice daily for 3 days), in which existence of an increased TIDA function has been demonstrated. FK 33–824 (0.5 mg/kg i.p.) increased significantly plasma PRL levels in control rats but failed to do so in TP rats and it elicited a significantly lower PRL response than in controls in rats treated with oPRL. In both experimental models, a PRL secretagogue, e.g. 5-hydroxytryptophan (50 mg/kg i.p.), elicited the same response as in controls, indicating that the pituitayr PRL pool was preserved. Kinetic characteristics of opioid binding sites in the hypothalamus of hyperprolactinemic rats did not differ from those of controls, and also hypothalamic Met-enkephalin concentrations were similar to those of controls. These findings would exclude a defect of endogenous opioid neurotransmission as responsible for the impaired PRL stimulation by the enkephalin analog. Supporting this were the findings that oPRL-treated rats exhibited a growth hormone response to FK 33–824 and a rise in plasma luteinizing hormone after naloxone (5 mg/kg s.c.) similar to those present in controls. These data indicate that the defective PRL responsiveness to opioids has to be attributed to the impairment of a neurotransmitter e.g. DA, functionally located at a site ‘downstream’ from opioid receptors. As already shown for oPRL-treated rats, TP rats exhibited a faster turnover rate of DA in the median eminence of the hypothalamus. In keeping with the idea that the hypothalamic dopaminergic system was involoved in the defective PRL responsiveness to opioids, Dom (50 μg/kg i.p.) induced aignificantly lower increase of PRL levels in TP and oPRL-injected rats than in controls. All these data demonstrate that opioid peptides and DA receptor antagonists are unable to discriminate the functional state of TIDA system. In fact, they fail to elicit a rise in plasma PRL in hyperprolactinemic states related to either TIDA hypo- (PST rats and humans) or hyperfunction (TP and oPRL-treated rats). In contrast to FK 33–824 and Dom, Nom (10 mg/kg i.p.), a drug which fails to lower PRL secretion in animals and patients with prolactinoma, did suppress plasma PRL levels of oPRL-treated rats as those of controls. The latter data indicate that indirectly acting DA agonists can discriminate the functional state of TIDA system; they fail to lower PRL secretion only when TIDA function is defective.

Progesterone administration prolongs the inhibitory effects of hyperprolactinemia on luteinizing hormone secretion in acutely ovariectomized rats.

Several studies have shown that hyperprolactinemia in rats inhibits the post-gonadectomy rise in plasma luteinizing hormone (LH) for a limited period only. In intact rats the suppression of plasma LH during hyperprolactinemia is more prolonged. In the present study we have examined the possibility that the elevated levels of progesterone brought about by the raised plasma prolactin levels in intact rats are involved in the maintenance of LH inhibition. We have observed the effect of exogenous progesterone administration during the early post-ovariectomy period on plasma LH levels in female rats made hyperprolactinemic by administration of the dopamine antagonist, domperidone. Following ovariectomy of virgin, female rats, plasma LH was determined on each day from Day 3 to Day 10 after ovariectomy. In control rats plasma LH had increased by approximately 5-fold during the period of the experiment. In control rats treated with progesterone the rise in plasma LH was inhibited temporarily but LH had increased to similar levels to the controls by Day 10. In hyperprolactinemic rats LH was suppressed until Day 7, after which significant rises were observed. However, in hyperprolactinemic rats treated with progesterone, LH did not rise in a similar fashion, and remained low throughout the experiment. We conclude that a combination of hyperprolactinemia and raised plasma progesterone concentrations is necessary for the continued inhibition of LH release after ovariectomy.

Plasma gonadotrophins profile in relation to body composition in underprivileged boys.

Abstract. The plasma concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured in 250 underprivileged boys (UP boys) aged 9.0 to 15.9 years living in a State orphanage and in 357 clinically healthy boys of the same age (with weight and height between the 3rd and 97th percentile for Mexican standards) and correlated with chronological age (CA), weight, height and calculated lean body mass (LBM) and total body fat (TBF). On a group basis, UP boys had a 2 years delay in the onset of clinical signs of puberty as well as a mild degree of malnutrition. In both groups of boys, the mean weights at time of initiation of the adolescent growth spurt in weight and at time of peak velocity of weight gain were very close to each other and similar to the values reported for Caucasian boys. The same phenomenon was true for their heights and the amounts of LBM and TBF (whether as an absolute value or as a percentage of body weight). Based on CA mean plasma FSH concentrations in UP boys were lower than normal from 11.0 to 13.9 years and the subsequent steep rise of this hormone occurred 2 years later than in healthy boys; however, when analyzed as a function of body weight, height or LMB, no such quantitative or qualitative differences emerged. On the other hand, mean plasma LH concentrations in UP boys were higher than in healthy boys only up to certain CA (&lt; 12.9 years), weight (&lt; 42.9 kg), height (&lt; 147.0 cm), LBM (&lt; 35.0 kg) or TBF (&lt; 9.0 kg); however, no steep rise in plasma LH was observed in contrast to healthy boys. Therefore, although from a chronologic view point UP boys had a delayed onset in plasma gonadotrophins changes, they did occur in association with the attainment of similar weight, height and LBM as in healthy boys. This observation seems to support further the hypothesis of a close association between a 'critical' level of LBM (and not body fat) and the initiation of puberty, both in healthy and multiply deprived boys.

The relationship of plasma gonadotrophins and steroid concentrations to body growth in girls.

Plasma concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), 17 alpha-hydroxyprogesterone (17 alpha-OHP), 17 beta-oestradiol (Oe2) and progesterone (P) were measured in 352 healthy girls aged 6.0 to 15.9 years, as a function of age (CA), weight, height and calculated lean body mass (LBM) and total body fat (TBF). The earliest hormonal changes were a fall in mean plasma FSH concentrations together with a small but significant rise in plasma Oe2 well in advance of any sign of pubertal development. The next changes were a progressive rise in plasma FSH and 17 alpha-OHP concentrations without further increments in plasma Oe2; these changes corresponded to a mean body weight of 29.8 kg, a mean height of 132.0 cm (initiation of the adolescent growth spurt), a mean LBM of 24.7 kg and a mean TBF of 5.1 kg. The last events were a progressive rise in plasma LH and Oe2 and less marked in P, which occurred in association with a mean body weight of 40.0 kg, a mean height of 142.0 cm (time of peak velocity of weight and height gain), a mean LBM of 31.8 kg and a mean TBF of 9.1 kg. Significant quadratic equations were disclosed between plasma FSH and LH versus CA, weight, height and LBM, and a significant linear correlation was observed between each gonadotrophin and TBF. These results show an association, not necessarily causal, between a 'critical level' of body composition and hormonal changes at the start of the adolescent growth spurt, as well as with late hormonal events at the time of peak velocity in weight and height gain. On the other hand, LBM rather than TBF seems more closely associated with the initiation and progression of puberty.

Effects of hypothalamic arcuate nucleus lesions on pulsatile luteinizing hormone concentration in ovariectomized rats.

We investigated the effects of hypothalamic arcuate nuclei destruction on the postovariectomy rise in plasma luteinizing hormone (LH) concentration and the pulsatile LH release mechanism in ovariectomized rats. Rats were injected with 1, 2, or 4 mg/g body wt of L-monosodium glutamate (MSG) on Days 1, 3, 5, 7, and 9 of life to lesion the arcuate nuclei. They were then ovariectomized as adults and used 2 or 4-8 weeks later. Serial blood sampling at 10-min intervals and measurement of plasma LH concentration revealed elevated plasma LH levels which fluctuated in a pulsatile fashion in all control and 1 and 2 mg/g/MSG-treated rats. In 4 mg/g MSG-treated rats, plasma LH levels were lower than in controls of both time periods after ovariectomy due to a decrease in the amplitude and/or frequency of LH pulses. Phenobarbital was administered to all 4- to 8-week ovariectomized rats to block endogenous pulsatile LH release. In phenobarbital-blocked rats, three sequential iv injections of LH releasing hormone (LHRH) caused substantial elevations in plasma LH concentrations even in the 4 mg/g MSG-treated animals which had low plasma LH concentrations during control bleedings prior to the injection of phenobarbital. The results indicate that the postovariectomy rise in plasma LH concentration and the associated pulsatile LH release mechanism are functional in rats with extensive arcuate nucleus lesions. The diminution in the rise in plasma LH levels and the decreased amplitude and/or frequency of LH pulses in the MSG-treated rats is likely due to a diminution in hypothalamic LHRH release.

The relationship of plasma gonadotropins and androgen concentrations to body growth in boys.

Abstract. Plasma concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), 17 alpha-hydroxyprogesterone (17α-OPH), androstenedione (Δ4) and testosterone (T) were measured in 543 healthy boys aged 6.0 to 15.9 years (with weight and height between the 3rd and 97th percentile for Mexican standards) as a function of chronologic age (CA), weight, height, surface area (SA) and calculated lean body mass (LBM) and total body fat (TBF). The earliest hormonal event was a clear rise in plasma 17α-OHP, either prior or simultaneously to at steady increase in plasma FSH, far ahead of any sign of puberty. These changes were closely followed by a continuous rise in plasma Δ4. Thereafter, there was a prolonged period of low but progressively increasing plasma FSH levels in the face of constantly low LH levels. However, a brisk rise in plasma LH and FSH occurred at a mean weight of 35.4 kg, at a height of 144.5 cm and when LBM was 32.0 kg. Simultaneously, plasma 17α-OHP began to fall, Δ4 reached a plateau and soon after, a marked rise in plasma T was documented. When plasma LH and FSH concentrations were plotted against CA, weight, height, SA and LBM a significant quadratic equation was disclosed in each case. Both gonadotrophins did not correlate with TBF. Multiple variance analysis demonstrated that LBM and SA had the most marked effect on LH, while LBM was the most important variable affecting plasma FSH concentrations. The present data suggest the association between a "critical level" of body composition and the major hormonal events in boys, regardless of a cause-effect relationship. A critical level of LBM (20–23 kg) and not of TBF was attained at time of the initial hormonal changes, as well as at the time of the major changes in plasma gonadotrophins (32–35 kg).

Interaction of luteinizing hormone-releasing hormone, cyproterone acetate and arginine vasotocin on plasma levels of luteinizing hormone in intact and castrated adult male rats

Treatment of unanesthetized castrated adult male rats every 3 h for 48 h with either 5 μg of arginine vasotocin (AVT) and/or 1μg luteinizing hormone-releasing hormone (LRH) caused a significant inhibition of plasma levels of luteinizing hormone (LH) compared to castrated control rats receiving diluent only. However, the intravenous (iv) injection of 1 μg of AVT into urethane-anesthetized male rats which had been castrated for 0, 24 or 48 h did not affect plasma levels of LH at 10, 20 or 60 min following injection compared to their respective diluent-treated castrated control rats. Similarly, the iv injection of either 100 ng, 1 μg or 10 μg AVT was unable to acutely affect plasma levels of LH in intact male rats. Following the iv injection of 2 doses of 50 ng LRH spaced 1 h apart in anesthetized castrated male rats, 2 peaks of equal magnitude in plasma LH were noted. Castrated rats treated with 2 injections spaced l h apart of LRH + AVT had significantly higher plasma levels of LH than did rats treated with LRH alone. In subsequent studies, both AVT and arginine vasopressin were observed to augment the plasma response of LH to an injection of LRH whereas oxytocin had no effect. A single injection of AVT + LRH significantly augmented the plasma titers of LH compared to levels observed in LRH-treated control rats as did a second injection l h later. The administration of cyproterone acetate sc for 2 days by itself had no effect on plasma LH but in conjunction with LRH caused a marked rise in plasma LH compared to intact rats treated with LRH alone. AVT in combination with LRH and cyproterone acetate caused a significant elevation in plasma LH at 60 min post-injection when compared to plasma levels of rats treated with LRH alone or the combination of LRH and cyproterone acetate. It is concluded that acute intravenous injections of AVT augment the LH-releasing activity of LRH; chronic treatment for 48 h, however, with LRH + AVT leads to a significant depression of plasma LH perhaps due to an exhaustion of the releasable pool of LH in the anterior pituitary.

The luteinizing hormone-releasing hormone (LH-RH) neuronal networks of the guinea pig brain. II. The regulation on gonadotropin secretion and the origin of terminals in the median eminence

Cell bodies synthesizing LH-RH are located throughout the central nervous system including the hypothalamic arcuate nucleus, the medial preoptic area and medial septal nucleus. The contribution of each of these cell groups to the LH-RH terminals in the median eminence was assessed by immunocytochemistry following placement of radiofrequency lesions in male guinea pigs. Lesions in the arcuate nucleus resulted in an almost complete absence of LH-RH fibers in the median eminence. Lesions in the medial preoptic area or suprachiasmatic nucleus produced a decrease in the amount of immunoreactivity throughout the median eminence; but there was only a small decrease in the numbers of labeled fibers, which was localized to the internal zone of the median eminence and the external zone on the ventral and lateral surfaces of the infundibular stalk. Lesions of the mammillary bodies, medial amygdaloid nucleus, septal nucleus and fornix had no effect. The effects of these lesions on pituitary gonadotropin secretion was also assessed. Only lesions in the arcuate nucleus diminished plasma concentrations of luteinizing hormone (LH) and testosterone in the male guinea pigs. Similary only arcuate lesions prevented the postcastration rise in plasma LH in ovariectomized female guinea pigs. These data strongly suggest that the arcuate nucleus is the major but not the sole source of LH-RH terminals in the median eminence, and these are responsible for the neural regulation of tonic gonadotropin secretion.

Pituitary responsiveness to luteinizing hormone-releasing hormone in insulin-dependent diabetes mellitus.

Impaired fertility and menstrual disturbances are common in diabetes mellitus. In order to study the effect of diabetes on gonadotropin secretion by the pituitary gland, twenty premenopausal diabetic females and seven diabetic males were investigated using luteinizing hormone-releasing hormone (LH-RH). Although the gonadotropes responded to LH-RH in the patients studied, a relative impairment was apparent when compared to normal matched control groups. In the female diabetic patients there was no difference in the gonadotropin responses obtained in those with oligomenorrhea or amenorrhea when compared to those with normal menses. A significant inverse relationship was found between the maximum rise in plasma luteinizing hormone and the fasting plasma glucose. These findings suggest an influence of glucose metabolism on pitiutary gonadotropin function. However, the reduced gonadotropin response is unlikely to be the sole cause of the abnormal gynecologic function.