Exposure to alcohol in utero alters the adult patterns of luteinizing hormone secretion in male and female rats

Luteinizing hormone (LH) secretory patterns were characterized in adult male and female rats exposed to ethanol during the last week of fetal life. Gonadectomized fetal alcohol exposed (FAE) males and females had significantly reduced plasma LH titers as compared to those of pair-fed (PF) controls. The phasic afternoon LH secretory response to estrogen and progesterone priming was also significantly reduced in FAE females. These differences do not appear to be a result of altered pituitary sensitivity to luteinizing hormone releasing hormone (LHRH), since the infusion of LHRH resulted in an equal response in PF and FAE females. Subsequent characterization of the episodic pattern of LH secretion in FAE males revealed significantly reduced mean LH level as well as a decreased pulse amplitude and frequency when compared to PF males. Taken together, these data indicate that some of the central mechanisms controlling pituitary LH secretion are altered by prenatal exposure to alcohol.     

Effects of applying gamma-aminobutyric acid(B) drugs into the medial basal hypothalamus on basal luteinizing hormone concentrations and on luteinizing hormone surges in the female sheep

Prior investigations have shown that localized infusion by microdialysis of gamma-aminobutyric acid(B) (GABA(B)) agonists into the medial basal hypothalamus of male sheep rapidly increases GnRH and LH pulse amplitude. The objectives of these studies were to determine if infusion of GABA(B) agonists SKF 97541 or baclofen into the medial basal hypothalamus of female sheep would affect basal LH secretion and if infusion of a potent antagonist would alter expression of LH surges induced by injection of estrogen. Infusion of either SKF 97541 (10 or 40 microM) or baclofen (1 mM) into estrogen-treated ovariectomized ewes did not alter basal LH secretory patterns, whereas both drugs significantly elevated mean LH and LH pulse amplitude in ovariectomized ewes during the nonbreeding season. Infusion of the antagonist CGP 52432 (250 or 500 microM) did not affect expression of estrogen-induced LH surges in ovariectomized ewes. These observations support the concept that GABA(B) receptors in the medial basal hypothalamus regulate basal LH secretion but do not regulate the surge mode of LH secretion in the female sheep.     

Equine luteinizing hormone possesses follicle-stimulating hormone activity in hypophysectomized female rats

The ability of equine luteinizing hormone (eLH) to promote follicular growth and maturation in hypophysectomized rats has been assessed. A single injection of equine LH has been shown to promote the growth of a large number of antral and preovulatory follicles. In addition, equine LH markedly increased serum estrogen levels and uterine weight. Furthermore, equine LH, like equine chorionic gonadotropin (eCG; PMSG) was able to significantly enhance the incorporation of [3H]thymidine into ovarian DNA, an activity shown to be specific to hormones having follicle-stimulating hormone (FSH) activity. Equine LH treated with an FSH antibody immunoaffinity column to remove any possible contamination still exhibited the above activity, demonstrating that the FSH activity is intrinsic to the eLH molecule. Equine LH has also been shown to be capable of inducing LH receptors in granulosa cells of ovaries of hypophysectomized rats, an activity specific to FSH-like hormones. From the doses required of eLH and the degree of response observed, it is concluded, however, that eLH in the hypophysectomized rat is less active than eCG as an FSH.     

Enhanced luteinizing hormone release by luteinizing hormone-releasing hormone in incubating female turkeys (Meleagris gallopavo)

To determine what role pituitary responsiveness plays in the suppression of gonadotropin level during incubation in the turkey, the ability of the pituitary to release luteinizing hormone (LH) in response to luteinizing hormone-releasing hormone (LHRH) was compared in incubating, laying, and photorefractory birds. In all three groups, the i.m. injection of LHRH (4 micrograms/kg) increased serum LH levels; however, the LH response was markedly enhanced in the incubating turkeys as compared with the laying (6.6-fold increase over preinjection levels vs. 1.9-fold; p less than 0.05) or the photorefractory birds (9.7-fold vs. 3.1-fold; p less than 0.05). The LHRH-induced LH release was also determined in turkeys as they shifted from the laying to the incubating phase of the reproductive cycle. This response increased (p less than 0.05) in magnitude as the birds started to incubate. The high prolactin level of incubating turkeys does not have a depressing effect on LHRH-stimulated LH release; thus, impaired LH response to LHRH is not a mechanism involved in the diminished gonadotropin secretion of incubating turkeys.     

N-methyl-d, l-aspartate stimulates growth hormone but not luteinizing hormone secretion in the sheep

The objective of this experiment was to determine the effects of N-methyl-d, l-aspartate (NMA) on luteinizing hormone (LH) and growth hormone (GH) secretion in castrated male sheep. Blood was sampled from Hampshire wethers every 15 min for 8 hr on day 1. At 4 and 6 hr after the initiation of the experiment, wethers were treated i.v. with NMA at a dose of 12 mg/kg body weight (n = 5) or .9% saline (n = 5). The dosage of NMA was within the range of doses that was previously demonstrated to stimulate LH secretion in monkeys. Blood samples were also collected every 15 min for 1 hr on day 2, beginning 24 hr after the first injection of NMA or saline. Treatment with NMA had no effect on mean LH concentrations, LH pulse frequency or LH pulse amplitude during the 4 hr period following the first injection on day 1. On day 2, however, mean LH concentrations were lower (p less than .01) in NMA versus saline-treated wethers. Conversely, administration of NMA evoked a dramatic increase (p less than .02) in mean GH concentrations on day 1. The mechanisms responsible for the effects of NMA described herein and whether or not these effects are relevant to the physiological control of LH and GH release in the sheep warrants further scrutiny.     

Reproductive experience and opioid regulation of luteinizing hormone release in female rats

The objective of the present study was to determine whether reproductive experience that produces shifts in opioid regulation of prolactin secretion and behavioural functions also alters opioid regulation of LH during the oestrous cycle or lactation. In Expt 1 the effect of naloxone administration (i.v.) on LH was compared between age-matched, nulliparous and primiparous, catheterized female rats on dioestrus II. In Expt 2, the effects of multiple reproductive experiences on opiate control of LH were investigated using cyclic, nulliparous and multiparous (three litters) rats. In both experiments, no differences in naloxone-stimulated LH release were found between groups even though multiple reproductive experiences resulted in the prolongation of oestrous cyclicity. In Expt 3, day 8 lactating primiparous rats were administered 2, 5, 10 or 25 mg naloxone kg-1 i.v. The three lowest naloxone doses, but not the 25 mg kg-1 dose, significantly increased LH concentrations. The possible effects of prior reproductive experience on opioid control of LH during lactation were then investigated. Naloxone at 0.5 mg kg-1, but not at 2 mg kg-1 or 10 mg kg-1, stimulated a significantly greater rise in LH in multiparous (two litters) than in primiparous females. Overall, these data indicate that while modest differences were found in naloxone-induced LH responses between multiparous and primiparous animals during lactation, reproductive experience did not significantly alter opioid regulation of LH during subsequent oestrous cycles at the naloxone doses examined. Hence, the effects of reproductive experience on opioid regulation of LH are less pronounced than those previously found for opioid regulation of prolactin and behaviour.     

Plasma androstenedione after injections of dexamethasone and luteinizing hormone releasing hormone in young post-pubertal bulls

This study was performed on six French Friesian bulls (aged 12 months at the onset of the experiment) on two separate occasions, 3 months apart and lasting 2 days each time. On each of both occasions, three bulls were submitted on the first day to an i.m. injection of dexamethasone (DXM, 20 mg) 6 h priot to a Luteinizing Hormone Releasing Hormone (LH-RH) challenge (0.250 mg i.m.) and the three others (control animals) to LH-RH only. On the second day, they all received a single LH-RH injection. The treated animals then served as controls on the second occasion and the controls as DXM—LH-RH treated individuals. Blood samples were taken at hourly intervals before LH-RH treatment (for 5 h), then every 15 min (for 2.5 h), and afterwards, every hour for 3 h.Androstenedione concentrations were significantly enhanced after LH-RH challenge in a similar manner on days 1 and 2 within groups, but the relative magnitude of the response in terms of area under the curve (ng/ml of plasma × 150 min) was lower in the DXM—LH-RH treated group than in the controls. In addition, the individual correlation between the testosterone and androstenedione responses was significant (P <0.05) in those animals treated but not in the controls. This study therefore suggests evidence of a double origin for androstenedione secretion, from the testes and probably from the adrenals.     

Divergent effects of leptin on luteinizing hormone and insulin secretion are dose dependent

We have shown recently that fasting permits leptin to modulate both luteinizing hormone (LH) and insulin secretion in cows. In rodents, leptin causes divergent effects on LH and insulin release that are dose dependent. To test the hypothesis that leptin effects on LH and insulin secretion in fasted cows are dose related, we examined the effects of various doses of recombinant ovine leptin (oleptin) in mature cows. Twenty ovariectomized beef cows, each bearing an estradiol implant to maintain basal estradiol concentrations, were used. All cows were fasted for 60 hr with free access to water and were assigned randomly to one of four groups (n = 5/group): 1) saline control; 2) leptin, 0.2 microg/kg; 3) leptin, 2.0 microg/kg; and 4) leptin, 20 microg/kg body wt. Blood samples were collected at 10-min intervals for 6 hr on Days 0 and 2, with saline or oleptin injected intravenously immediately after the first intensive sample on Day 2 (54 hr). Leptin caused a dose-related increase (P < 0.001) in mean concentrations of circulating LH. Stimulation of LH release by leptin was significant at the lowest (141% of control) and middle (122% of control) doses used, but no increase was observed for the highest dose. Increased mean concentrations of LH appeared to result from an augmentation of basal secretion, as pulse characteristics were not affected. After 54 hr of fasting, plasma insulin concentrations were lowered (P < 0.01) in all treatment groups compared to Day 0. After leptin injections, plasma insulin concentrations increased (P < 0.01) and reached highest concentrations during the first hour of sampling. However, this increase was sustained for several hours only in the intermediate (2.0 microg/kg) dose group. Collectively, our results show that leptin has potent positive effects on both LH and insulin secretion in fasted cows, but the anterior pituitary and endocrine pancreas appear to become downregulated in the presence of excess ligand.     

Effect of phenoxybenzamine on luteinizing hormone release in the female rat

To clarify the mode of action of phenoxybenzamine, an alpha adrenergic blocking agent, its effects upon plasma LH levels in ovariectomized rats and upon the ovulatory LH surge expected between 1400 and 1600, the critical period, on the day of proestrus in normal rats were studied. A single injection of phenoxybenzamine, 20 mg/kg, given at 1300 on the day of proestrus bokced ovulation (1 out of 7 ovulating), while plasma LH did not differ from controls between 1500 and 1600. An additional injection of 20 iu HCG at 1500 prevented the ovulation block (83% ovulating). A single phenoxybenzamine injection at 1700 failed to prevent ovulation (5 out of 7 ovulating). The beta adrenergic blocking agents, propanolol and MJ 1999, did not affect ovulation. Treatment with phenoxybenzamine for 2 days, 20mg/kg/day, for 8 days, 10mg/kg/day, were did not prevent the rise causing a reduction in blood flow through the ovary rather than acting as a neurogenic stimulus in the hypothalamus.     

Coital stimuli controlling luteinizing hormone secretion and ovulation in the female ferret

A series of experiments focused on the masculine coital behaviors controlling pituitary luteinizing hormone (LH) secretion and reflex ovulation in the estrous female ferret. An initial experiment investigated which coital stimuli from the male are required to induce ovulation. It was found that corpus luteum formation, which served as an index of ovulation, occurred in estrous female ferrets only if the male achieved a penile intromission. Neck gripping, mounting, and pelvic thrusting behavior without intromission by the male failed to induce ovulation. A second experiment investigated the timing and magnitude of the coitus-induced LH surge associated with ovulation. Blood was obtained via jugular catheters from estrous females in various mating situations. Plasma LH concentrations were measured by a heterologous radioimmunoassay that was validated for use in the ferret. A significant surge in plasma LH occurred only when an intromission was achieved by the stud male. Plasma LH was significantly elevated 2.0 h after the introduction of the male, peak values were reached 6.0 h later, and this elevation lasted on average 5.7 hours (5/5 females). No LH rise occurred in 2/2 female ferrets in which only neck gripping, mounting, and pelvic thrusting, but no intromission, were allowed to occur. The ferret mating pattern and the resultant LH response differ from those seen in three other induced ovulators (cat, vole, and rabbit) in which the male's intromission latency and duration are much shorter than in the ferret, and in which a distinctive peak in plasma LH often occurs within 1 h after mating.     

Role of estradiol in inducing an ovulatory-like surge of luteinizing hormone in sheep

Two experiments were performed to examine the effect of estradiol on secretion of luteinizing hormone (LH) and on the number of receptors for gonadotropin-releasing hormone (GnRH) after down regulation of GnRH receptors in ovariectomized ewes. In the first experiment, ovariectomized ewes were administered one of four treatments: Group 1) infusion of GnRH i.v. for 40 h; Group 2) injection of 100 micrograms estradiol i.m.; Group 3) infusion of GnRH i.v. for 16 h followed immediately by an injection of 100 micrograms estradiol i.m.; and Group 4) infusion of GnRH i.v. for 40 h plus injection of 100 micrograms estradiol i.m. after the 16th h of infusion. Ewes in Groups 1, 3 and 4 responded to the infusion of GnRH with an immediate increase in serum concentrations of LH, with maximum values occurring between 2 and 4 h after the start of infusion; serum concentrations of LH then began to decline and were approaching the pretreatment baseline within 16 h. Administration of estradiol resulted in a surge of LH regardless of whether the pituitary had been desensitized by infusion of GnRH or not. In all cases the magnitude of the surge was similar to that induced by the initial infusion of GnRH. In Groups 2 and 3 the surge of LH began at 12.3 +/- 0.1 and 11.9 +/- 0.1 h after administration of estradiol. In contrast, the ewes in Group 4 had a surge of LH beginning 3.7 +/- 0.1 h after administration of estradiol.(ABSTRACT TRUNCATED AT 250 WORDS)     

Expression and localization of luteinizing hormone receptor in the female mouse reproductive tract

The presence of the LH receptor (LHR) in nongonadal tissues of the reproductive tract has been reported, but localization studies have not been performed. Our objectives were to demonstrate the presence of LHR in the reproductive tract and to localize receptor expression. Reproductive age rats and mice were obtained and (125)I-hCG binding assays were performed on membrane preparations from the uterus, ovary, liver, and testis. In situ hybridizations were performed using (35)S-labeled antisense and sense RNA probes prepared from nucleotides 1-591 of the mouse LHR cDNA. Specific hCG binding was detected in membrane preparations from the ovary, uterus, and testis but not in the liver in both the rat and mouse. In the ovary, LHR mRNA was localized in theca cells, large follicles, and corpora lutea as expected. In the uterus, LHR mRNA was expressed in stromal cells of the endometrium and in the uterine serosa. Uterine smooth muscle cells had low levels of expression, and the endometrial epithelium was negative. In the oviduct, high levels of LHR expression were noted on the serosa and in subepithelial cells. Oviductal smooth muscle had low expression, and the epithelium was negative. We conclude that functional, nongonadal LHR are expressed in the mouse reproductive tract. The presence and localization of LHR expression in the mouse reproductive tract lay the foundation for transgenic models to address the physiologic role of these receptors.     

Simultaneous measurement of luteinizing hormone-releasing hormone and luteinizing hormone during estradiol-induced luteinizing hormone surges in the ovariectomized ewe

Sequential bleeding and push-pull perfusion of the hypothalamus were used to characterize luteinizing hormone (LH) and LH-releasing hormone (LHRH) release in ovariectomized (OVX) ewes after injection of corn oil or estradiol benzoate (EB). Push-pull cannulae were surgically implanted into the stalk median eminences of 24 OVX ewes. Seven to 14 days later each of 20 animals was given an i.m. injection of 50 micrograms EB. Blood samples and push-pull perfusate were collected at 10-min intervals for 6-12 h beginning 12-15 h after EB injection. Four OVX ewes were given i.m. injections of corn oil 7 days after implantation of push-pull cannulae. Blood samples and push-pull perfusate were collected at 10-min intervals for 4 h between 18 and 22 h after injection of corn oil. Luteinizing hormone remained below 2 ng/ml throughout most of the sampling periods in 9 of 20 EB-treated ewes. In 5 of these 9 LHRH also was undetectable, whereas in 4 LHRH was detectable (1.84 +/- 0.29 pg/10 min), but did not increase with time. Preovulatory-like surges of LH occurred in 11 EB-treated ewes, but LHRH was undetectable in 5. In 4 of 6 ewes showing LH surges and detectable LHRH, sampling occurred during the onset of the LH surge.(ABSTRACT TRUNCATED AT 250 WORDS)     

Peripheral leptin administration alters hormone and metabolite levels in the young pig

The present study was conducted to determine if peripheral leptin administration can alter GH secretion or feed intake in young pigs. Six, 6 kg female pigs were fasted overnight and randomly chosen to receive porcine recombinant leptin or saline injections in a crossover design. Three leptin dosages were tested over a 10 day period, 100, 200 or 500 microg/kg body mass (L100, L200 or L500). Leptin was administered in 0.2% bovine serum albumin as a bolus injection into the carotid artery. Blood samples were obtained from the jugular vein over a 24 h period. Leptin delayed feeding in pigs treated with L200 and L500 (P<0.05), while reducing overall intake in pigs treated with L100 (P<0.05). L200 or L500 depressed blood glucose (P<0.05). Plasma insulin levels were elevated by feeding in control animals, while insulin levels were depressed in pigs treated with L200 or L500 (P<0.05). L200 elevated plasma growth hormone (P<0.05) with three peaks apparent at 5, 8, and 13 h post injection. The ability for a single injection of leptin to produce significant changes in hormone and metabolite levels suggests that this peptide has a role in regulation of peripheral metabolism.