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PubMed1980

The effect of an antiserum to luteinizing hormone-releasing hormone on the progesterone-induced luteinizing hormone surge in ovariectomized, estrogen-primed rats.

A rabbit antiserum to synthetic LHRH was shown to be specific to rat hypothalamic LHRH, as revealed by binding studies (RIA). The present study was undertaken to determine the effects of this antiserum (LHRH-AS) on the progesterone-induced LH surge in ovariectomized rats primed with estrogen on the proestrous LH surge in cycling females. An ip injection of 0.2 ml LHRH-AS at 1200 h on proestrus completely inhibited the preovulatory rise in serum LH from 1700-1800 h. In long term ovariectomized rats, a sc injection of estradiol benzoate reduced serum LH levels by 50% at 1200 h on the third day. Subsequent administration of progesterone elicited a LH surge, with peak LH value 4-6 h after progesterone. However, concurrent administration of LHRH-AS effectively prevented the increase in LH release by progesterone, and an iv injection of LHRH-AS was shown to be more effective than ip administration in inhibiting the progesterone stimulation of LH release. Although estrogen and progesterone may induce a change in pituitary responsiveness to hypothalamic LHRH in ovariectomized rats, the present study provides evidence that tonic and/or increased LHRH release is required for the acute increase in LH release caused by progesterone.

Animals↗
PubMed1980

Multiple inhibitory actions of luteinizing hormone-releasing hormone agonist on luteinizing hormone/human chorionic gonadotropin receptor-mediated ovarian responses.

The administration to female rats of the LHRH agonist, [des-GlyNH2(10)]LHRH ethylamide, as either a single dose or repeated injections resulted in a decrease in the binding of 125I-labeled hCG to ovarian plasma membranes. An ovarian cell suspension prepared from the agonist-injected group of rats also responded to hCG with a decreased ability to accumulate cAMP and progesterone compared with the saline-treated controls. The receptor loss was due to a decreased number of hormone-binding sites rather than to a change in the affinity of the receptor for the hormone. Preincubation of ovarian cells with the agonistic analog in vitro also caused an inhibition of progesterone synthesis in response to hCG, cholera toxin, and 8-Bromo-cAMP, suggesting a direct inhibitory effect of the analog on ovarian steroidogenesis. Prior exposure to the agonistic analog, however, had no effect on cAMP accumulation by the ovarian cells in response to either hCG or cholera enterotoxin, further suggesting that the site of inhibitory action lies at a point after cAMP accumulation. In summary, the present study demonstrates that 1) the inhibition of ovarian steroidogenesis observed in response to the injection of the LHRH agonist is primarily due to down-regulation of ovarian hCG/LH receptors with a resultant decrease in cAMP accumulation, and this effect may be caused by the pulses of LH release from the pituitary, and 2) the direct inhibitory effect on steroidogenesis observed under in vitro conditions is independent of gonadotropin receptor, and the site of this inhibitory action lies at a point after cAMP accumulation.

Animals↗
PubMed1981

In vitro effect of danazol on luteinizing hormone-releasing hormone-stimulated luteinizing hormone release in rat anterior pituitary cell cultures in vitro.

Monolayer cultures of anterior pituitary glands from female rats were exposed to 5 X 10(-6) M danazol for 0, 4, 24, 48, and 72 h in Dulbecco's Modified Eagle's Medium supplemented with 10% horse serum and 2.5% fetal calf serum. After this treatment, the cell cultures were rinsed and challenged with 10(-8) M LHRH for 6 h. The media were collected and assayed for LH by a hormone-specific RIA using the double antibody precipitation technique. A control incubation was carried out by exposing cell cultures for the same length of time in the absence of danazol but in the presence of 0.5% ethanol in which danazol was dissolved, then challenging the culture with 10(-8) M LHRH, as was done in the experimental group, and assaying the LH released in the medium. The results showed that exposure of cell cultures to danazol caused a significant decrease in LH release in response to LHRH from 13,800 +/- 500 to 3,500 +/- 200 ng/ml. The inhibition of LH release was dependent on both the duration of danazol exposure and its concentration. Danazol exposure had, however, little effect on basal LH secretion by the pituitaries, which remained at about 600 ng/ml at all time points examined. Under the experimental conditions, danazol exerted no effect on the incorporation of amino acid into protein in the cell culture. These results suggest that one of the mechanisms of the antigonadotropic effect of danazol is inhibition of the responsiveness of the pituitary to LHRH-induced LH release.

Animals↗
PubMed1982

Discriminative effects of testosterone on hypothalamic luteinizing hormone-releasing hormone levels and luteinizing hormone secretion in castrated male rats: analyses of dose and duration characteristics.

We have previously reported that in castrated male rats gonadal steroids can raise LHRH levels in the medial basal hypothalamus (MBH). However, there was an important dissociation between episodic LH release and the MBH LHRH response to 17 beta-estradiol. In the present study we have examined the effects of varying the dose of testosterone (T) on the MBH LHRH levels, episodic LH release pattern, and pituitary responsiveness to LHRH; in addition we have determined the duration of T exposure required to elicit the MBH LHRH response. Results show that low serum levels of T (413-638 pg/ml) were just as effective as higher concentrations (1337-1776 pg/ml) in raising the MBH LHRH levels at 96 h; the minimum duration of exposure to T was 72 h. However, whereas higher T levels (greater than 1 ng/ml) suppressed LH release coincident with elevated LHRH levels, low T concentrations did not alter LH release contemporaneous with the MBH LHRH elevations. Analysis of the episodic LH secretion pattern disclosed that these low concentrations of T changed neither the number of pulses per 3 h per rat, pulse amplitude, nor the interpulse interval. On the other hand, as T concentrations were increased, pulse amplitude fell in a dose-related manner while other components of episodic LH secretion remained unchanged. Despite these differential effects of T on the LH release pattern, pituitary sensitivity to exogenous LHRH was reduced by the low as well as high levels of T. These studies show that 1) T can activate those intracellular neurosecretory events that are involved in augmented LHRH supply to the nerve terminals in the median eminence; 2) T can stimulate LHRH accumulation in the MBH by mechanisms that may not involve inhibition of LHRH release; and 3) higher T levels do not alter LH pulse frequency but depress only the pulse amplitude that may result from decrements in the amounts of LHRH released with each neural episode and depressed pituitary sensitivity to LHRH.

Animals↗
PubMed1982

Simultaneous measurement of luteinizing hormone-releasing hormone and luteinizing hormone release in unanesthetized, ovariectomized sheep.

The push-pull perfusion technique was used in combination with a sequential bleeding schedule to estimate simultaneously the release patterns of LHRH and LH in unanesthetized ovariectomized sheep and to determine the temporal relationship between the release of these two hormones. Ovariectomized (greater than 30 days) ewes received unilateral push-pull cannula (PPC) implants (od, 0.85 mm) into the median eminence. After at least 6 days of recovery, each ewe was fitted with an indwelling jugular catheter. For push-pull perfusion, a stylette was removed from the outer PPC, and an inner cannula assembly (od, 0.40 mm) was inserted. Artificial cerebrospinal fluid was pushed through the inner cannula and pulled up between the cannulae at 20 microliters/min. Continuous 10-min perfusate fractions were collected, acidified, and stored at -20 C for LHRH RIA. Blood samples were obtained every 10 min via the jugular catheter, each being drawn 5 min after the start of a perfusate collection interval. Plasma LH levels were determined by RIA. The duration of the sampling was 3-7 h. LHRH output was distinctly pulsatile, occurring at a frequency of approximately one pulse every 30-40 min (n = 5 sheep). LHRH pulse amplitude and frequency remained relatively constant throughout each perfusion. Plasma LH values also were pulsatile, and all LH peaks occurred either during the same interval or during the interval after a LHRH pulse. LH pulses always were accompanied or directly preceded by LHRH pulses, but LHRH pulses were not always followed by LH pulses. The amplitudes of LH pulses and corresponding LHRH pulses were highly correlated (r = 0.81; P less than 0.01). Histological examination revealed that detection of LHRH in perfusates depended upon the placement of the PPC tip into either the zona externa of the central median eminence or adjacent areas. These experiments demonstrate that 1) hypothalamic LHRH release in the Ovx ewe occurs in discrete pulses, with a mean interpulse interval of 38.7 +/- 1.5 min, 2) LH pulses invariably are preceded or accompanied by LHRH pulses, and 3) LH pulse amplitude is highly correlated with LHRH pulse amplitude.

Animals↗
PubMed1983

The luteinizing hormone-releasing hormone (LHRH)-desensitized rat pituitary: luteinizing hormone responsiveness to LHRH in vitro.

Desensitization of the anterior pituitary has been observed after continuous infusion of LHRH or repetitive administration of LHRH at concentrations or frequencies exceeding physiological limits. We have studied the LH responsiveness of the LHRH-desensitized male rat anterior pituitary in a continuously perifused dispersed cell culture system. Infusion of 10 nM LHRH initially stimulated a 4- to 5-fold increase in LH secretion which became maximal at 6-9 min and which declined gradually to a preinfusion baseline over 6 h. Since the cells did not maintain peak levels of LH secretion in the presence of continuous exposure to LHRH, they were considered to be desensitized. These desensitized cells were studied to determine their LH responsiveness to LHRH. Cells desensitized by a 6-h LHRH infusion responded to four hourly LHRH boluses of 200 pm by releasing four statistically equal LH pulses. The response of desensitized cells to 200 pm LHRH was similar to that of 10 pm LHRH of nondesensitized cells. Furthermore, desensitized anterior pituitary cells responded to LHRH in a linear dose-dependent manner. The dose response of desensitized cells ranged from 75-500 pm, whereas for nondesensitized cells a dose response was observed from 1-75 pm. In addition, anterior pituitary cells desensitized with continuous LHRH infusion can respond to a second LHRH infusion of a greater concentration and become desensitized for a second time. These data suggest that the capacity of the pituitary gland to store and secrete LH while desensitized is similar to that of the nondesensitized anterior pituitary. The major difference between cells desensitized with LHRH and nondesensitized cells is that desensitized cells require a larger dose of LHRH to elicit a given LH response.

Animals↗
PubMed1983

Cortisol inhibits and adrenocorticotropin has no effect on luteinizing hormone-releasing hormone-induced release of luteinizing hormone from bovine pituitary cells in vitro.

Suckling causes a delay in onset of estrus and ovulation in cattle postpartum. In addition, the suckling stimulus causes the release of corticoids presumably via ACTH. Since any hormone released by suckling is a potential inhibitor of gonadotropin secretion and/or ovulation, we investigated the effects of ACTH and cortisol on LHRH-induced LH release from bovine pituitary cells in vitro. Anterior pituitary glands were obtained from cows killed during the luteal phase of an estrus cycle (days 5-15). Pituitary cells, disaggregated enzymatically, were grown in Dulbecco's medium containing 10% dextran charcoal-stripped fetal calf serum. On day 5, cultures were washed and reincubated in serum free medium containing the hormone being tested. After 6 h of incubation, LHRH was added in 10 microliters medium and incubation continued for an additional 6 h. ACTH at 4.3 X 10(-9), 4.3 X 10(-8), and 4.3 X 10(-7) M had no effect on basal or LHRH-induced LH release. Cortisol at 12.1 ng/ml decreased (P less than 0.001) the slope of LHRH response curve (b1 = 2.9 vs. 5.5 for controls). To determine if this effect was specific for cortisol, we compared cortisol, dexamethasone, and progesterone. LHRH-induced LH release (percent of control) was decreased (P less than 0.001) by 12.1 ng/ml cortisol (98%), 1, 5, and 10 ng/ml dexamethasone (60%, 71%, and 88%), but not by 3.1 ng/ml progesterone. The inhibitory effect of cortisol was reversible. Thus, LHRH-induced LH release (percent of controls) at 0, 24, 48, and 72 h after a 24-h exposure to 12.1 ng/ml cortisol was 19%, 89%, 100%, and 115%, respectively. We have demonstrated that cortisol at concentrations found normally in blood of cows postpartum will inhibit LHRH-induced LH release from bovine pituitary cells. This observation is consistent with the hypothesis that cortisol released by suckling may inhibit gonadotropin secretion postpartum and as such may prolong the anovulatory interval postpartum.

Adrenocorticotropic Hormone↗
PubMed1983

Prolactin suppresses luteinizing hormone secretion and pituitary responsiveness to luteinizing hormone-releasing hormone by a direct action at the anterior pituitary.

In pathological or experimental hyperprolactinemia, the elevated circulating levels of PRL are the usual cause of the impairment in gonadotropic function. The present study was undertaken to determine whether PRL could suppress basal LH secretion and LHRH-stimulated LH release by a direct action at the anterior pituitary. Anterior pituitaries from ovariectomized rats were incubated in medium 199 alone or in medium 199 containing ovine PRL, and basal and the LHRH-stimulated LH release were followed for 2 or 3 h in vitro. Ovine PRL at 40 and 80 micrograms/ml suppressed basal LH release by 41% and 72%, respectively, at 2 h of incubation. This suppressive effect of both concentrations of PRL continued to the third hour of incubation. LHRH at 5 ng/ml increased the release of LH from pituitaries incubated in medium alone by 57%, 61%, and 107% at 1, 2, and 3 h of incubation, respectively. However, in the pituitaries treated with 40 micrograms/ml ovine PRL, the stimulatory effects of LHRH were diminished at all time points measured. Pretreatment of anterior pituitaries with ovine PRL for 6 h significantly inhibited by 81% the LHRH (5 ng/ml) stimulation of LH release at 2 h of incubation. On the other hand, inhibition of endogenous PRL release by 10(-6) M bromocriptine enhanced the stimulatory effects of 5 ng/ml LHRH by 2.5-fold at 2 h of incubation. The inhibitory effects of PRL on basal and stimulated LH secretion appeared unique, since neither BSA nor vasopressin could elicit similar suppressive effects on LH. These results suggest that in anterior pituitaries exposed to elevated levels of PRL, LH secretion and pituitary responsiveness to LHRH could be impaired. This phenomenon may contribute in part to the antigonadotropic effects of PRL.

Animals↗
PubMed1983

Synthesis, luteinizing hormone-releasing activity, and receptor binding of chicken hypothalamic luteinizing hormone-releasing hormone.

Chicken hypothalamic LHRH, which was recently structurally characterized, was synthesized by solid-phase methodology, characterized, and tested for LH-releasing activity using anterior pituitary cells from chickens and sheep, as well as for binding to chicken and rat anterior pituitary membrane receptors. Synthetic chicken LHRH exhibited identical properties to the isolated natural chicken LHRH in several chromatographic systems. Synthetic chicken LHRH displayed identical activity to natural chicken LHRH in stimulating LH release from dispersed chicken anterior pituitary cells, and synthetic mammalian LHRH was equipotent in this system. Both the natural and synthetic chicken peptides had similar low potency in stimulating LH release from cultured ovine anterior pituitary cells (approximately 1% of the potency of synthetic mammalian LHRH). The ED50 of binding to rat anterior pituitary membrane receptors was 2.5 X 10(-6) M for synthetic chicken LHRH, compared to 6.3 X 10(-8) M for synthetic mammalian LHRH.

Animals↗
PubMed1983

Evidence that norepinephrine and epinephrine systems mediate the stimulatory effects of ovarian hormones on luteinizing hormone and luteinizing hormone-releasing hormone.

Results from previous investigations have suggested an important role for central epinephrine (EPI) systems in mediating the stimulatory effects of ovarian hormones on LH release in ovariectomized female rats. The purpose of these experiments was 1) to test whether selective inhibition of EPI synthesis blocks the sequential accumulation and decline of LHRH concentrations in the median eminence that precedes the ovarian hormone-induced LH surge and 2) to test whether the stimulatory ovarian hormone regimen enhances the activity of EPI systems in the hypothalamus. Ovariectomized rats were treated with estradiol, followed 2 days later by progesterone. Animals were treated before progesterone administration with saline, one of the EPI synthesis inhibitors [SK&F 64139 (2,3-dichloro-tetrahydroisoquinoline HCl) or LY 78335 (dichloro-alpha-methylbenzylamine)], or the dopamine-beta-hydroxylase inhibitor FLA-63 (bis-4-methyl-1-homopiperazinyl thiocarbonyl disulfide), which inhibits NE and EPI synthesis. The catecholamine synthesis inhibitors blocked or delayed the afternoon LH surge. FLA-63 completely prevented the accumulation of LHRH in the median eminence that preceded the rise in LH release. However, selective EPI synthesis inhibition with SK&F 64139 only partially prevented this increase in LHRH. A second EPI synthesis inhibitor, LY 78335, delayed both the LH surge and the rise in LHRH. In a second experiment, the administration of estradiol and progesterone to ovariectomized rats increased the alpha-methyltyrosine-induced depletion of hypothalamic EPI, suggesting increased activity in this system during the LH surge. Further experiments localized this effect to the medial basal hypothalamus. The depletion of both NE and EPI after synthesis inhibition was also enhanced during an earlier period, approximating the time of LHRH accumulation. These results suggest that the ovarian hormones activate both NE and EPI systems to stimulate the early afternoon rise of LHRH in the median eminence and to induce the subsequent LH surge.

Animals↗