Luteinizing hormone secretion as a response to a second naltrexone administration

Previous studies with naltrexone (Nalt), a "long-lasting" opioid antagonist, demonstrated a rapid increase in luteinizing hormone (LH) secretion which gradually declined, reaching baseline values after 1 hr. A second Nalt challenge, 120 min later, caused only a blunted response. This poor reaction has been shown in this study not to be due to lack of pituitary responsiveness, because LH-releasing hormone treatment revealed a normal response. A time-response study was carried out in order to establish the refractory period length, by administering a second Nalt injection at 0 hr (immediately after the first injection) and at 2, 4, 8, 16, and 24 hr after the first bolus. Partial responsiveness could be achieved 2 and 4 hr after the first challenge. However, only after 8 hr was a full response recorded. The diurnal changes in serum LH (nadir at 18.00 hr) did not affect the response to Nalt challenge. It is suggested that in the presence of a Nalt blockade, nonopioid systems are able to "normalize" LH blood levels. However, when Nalt blood levels have fallen sufficiently to allow the endogenous opioid system to take primary control again, then a second Nalt injection will provoke a renewed response.     

Opiate system involvement in the control of LH secretion in diabetic and normoglycemic male rats

The effect of Naltrexone (Nalt), a specific opiate receptor blocker, on LH secretion was studied at frequent intervals during the first hour following treatment. Nalt was injected i.v. by one bolus (1 mg/rat) to diabetic and normoglycemic rats. Blood samples (0.8 ml) were withdrawn at short intervals after injection, through an indwelling cannula. The diabetic rats responded by secretion of LH, which was lower, but not significantly, than that of normal rats, (peak levels 0.74 +/- 0.17 and 0.97 +/- 0.21 ng/ml respectively). After 45 min., LH levels were in the same range as baseline level in the diabetic group; but were still significantly elevated in the control rats. Thus, it can be concluded that in normal rats, as well as in diabetics, LH secretion as a response to Nalt was episodic in spite of Nalt's long half life time. In order to explain the rapid fall in LH levels after Nalt administration, normal rats were injected with a second bolus of Nalt, 2 hours after the first. The second bolus caused only a blunted response of LH secretion. In another experiment, administration of morphine (1 mg/rat) 2 hours after pretreatment with Nalt did not stimulate the prolactin secretion which normally follows morphine treatment. These results indicate that the rapid decrease of LH levels after Nalt treatment in normal rats is not due to absence of the drug in the system. It is suggested that other neural mechanisms, such as the dopaminergic system, are activated during Nalt influence.     

Effect of pimozide on the cytology of the eel pituitary

Pimozide, a specific blocker of dopaminergic receptors, was injected for 4 to 9 days in freshwater (FW) eels or eels acclimated to sea water (SW), for 10 to 30 days. The daily dose was 100 or 200 microgram/100 g. In FW, pimozide induces a nuclear hypertrophy in the prolactin (PRL) cells of eels; these elongated cells increase in height. The amount of erythrosinophilic granules in the cytoplasm, initially reduced, increases. Plasma electrolyte values are not modified: only the plasma sodium level slightly rises with the higher dose. In SW, PRL cells appear less active. After 10 days, this hypoactivity is not yet fully evident; pimozide stimulates PRL cells without affecting electrolyte values. After 1 month in SW, PRL cells are stimulated with pimozide and a slight regranulation may occasionally occur. The response in SW is never as marked as it is in FW; a high dose is not more effective than a low one. The higher dose significantly raises Na+, Ca2+ and Cl- plasma levels. These data suggest that prolactin synthesis and release increase with pimozide. They corroborate the hypothesis of a hypothalamic inhibitory control on PRL secretion mediated through dopaminergic fibers in the eel, but other factors may also be involved in this regulation in addition to the effect of salinity.     

Dermorphin decreases plasma LH levels in human: evidence for a modulatory role of gonadal steroids

The purpose of this study was to evaluate the effects of dermorphin, a new synthetic powerful opiate-like heptapeptide, on plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels in fertile and postmenopausal women. In fertile subjects, dermorphin (5.5 micrograms/kg min for 30 min) decreases plasma LH (p less than 0.01 vs. baseline and placebo values), but not plasma FSH. The area under the curve during dermorphin infusion was significantly lower than during placebo infusion (p less than 0.01). Pretreatment with the opioid receptor antagonist naloxone, blocked the decrease of plasma LH levels. In postmenopausal women not subjected to any treatment, dermorphin infusion did not significantly modify plasma LH and FSH levels. On the contrary, its administration to postmenopausal subjects treated with conjugated estrogens and medroxyprogesterone acetate significantly decreased plasma LH levels (p less than 0.01, vs. baseline, placebo and area under the curve). Considering the modulatory role exerted by ovarian steroids on the activity of such receptors, these data also indicate that opioid systems play a very important part in the hypothalamus-pituitary-ovarian axis.     

Site of action for β-endorphin-induced changes in plasma luteinizing hormone and prolactin in the ovariectomized rat

A number of sites have been hypothesized as loci at which opioid substances act to alter the secretion of luteinizing hormone (LH) and prolactin (PRL) (1–8). The aim of the present study was to determine the site(s) at which the opioid peptide β-endorphin (β-END) acts to influence plasma LH and PRL levels in the ovariectomized (OVX) rat. β-END, administered into the third ventricle of conscious OVX rats fitted with jugular catheters, significantly decreased plasma LH in doses ? 50 ng and increased PRL levels at all doses administered (10, 50, 100 and 250 ng) in a dose dependent fashion. To identify possible central nervous system sites of action, 250 ng β-END was unilaterally infused into various brain sites. Plasma LH was significantly decreased and plasma PRL significantly increased by infusions into the ventromedial hypothalamic area, the anterior hypothalamic area, and the preoptic-septal area. There was no significant effect of β-END infusions into the lateral hypothalamic area, amygdala, midbrain central gray, or caudate nucleus. When hemipituitaries of OVX rats were incubated $\text{in}$$\text{vitro}$ with β-END (10^?7M to 10^?5M), there was no suppression of basal or LHRH-induced LH release, nor was there any alteration of basal PRL release. It is concluded that β-END acts at a medial hypothalamic and/or preoptic-septal site and not the pituitary, to alter secretion of LH and PRL.     

Suppression of pimozide-induced prolactin secretion by piridoxine (vitamin B6)

I.V. administration of 300 mg. Pyridoxine caused an acute fall in prolactin (PRL) plasma levels in six normal subjects. Like levodopa, pyridoxine suppressed the increase in PRL secretion induced by treatment with pimozide, a specific dopamine receptor blocking agent. These findings further support the hypothesis that vitamin B6 stimulates dopaminergic activity at hypothalamic and/or hypophyseal level.     

Plasma levels of beta-endorphin, prolactin and gonadotropins in male athletes after an international nordic ski race

Plasma beta-endorphin, prolactin (PRL), FSH and LH were measured in 17 volunteer male subjects at rest and under the stress caused by a long-distance nordic ski race. The race induced increased levels of beta-endorphin and PRL in all skiers. The changes in PRL with exercise were significantly related to the changes in beta-endorphin (r = 0.69, p less than 0.001). Furthermore, the highly trained skiers training over 150 km.week-1 of nordic ski showed consistently higher post-exercise beta-endorphin and PRL levels than the moderately trained skiers who trained for 20 km.week-1. In addition the race induced slight falls in FSH and LH; however plasma gonadotropin levels did not show any correlation with plasma beta-endorphin concentrations and did not differ between the two groups of skiers. These results suggest that endogenous opioid peptides may modulate PRL secretion in heavy exercise, since they are of minor importance in the release of FSH and LH in such a situation. The observations also suggest that the degree of previous training and the exercise intensity do seem to be responsible for the hormonal changes.     

Effects of ovariectomy or force feeding on the plasma concentrations of prolactin and luteinizing hormone in incubating turkey hens

The effect of ovariectomy (OVX) on plasma concentrations of prolactin (PRL) and luteinizing hormone (LH) in incubating turkey hens was studied. Neither the sham-operated nor the OVX hens exhibited any change in the pattern of incubation behavior as a result of the surgery. Plasma concentrations of estradiol decreased to less than approximately 3 pg/ml by 2 days after surgery in the OVX hens. There were no significant differences in plasma levels of PRL between the sham-operated and OVX hens throughout the study. The concentration of PRL did not change in either the sham-operated or OVX hens and was maintained at high levels after surgery and during incubation of the eggs. By 2 days after hens were placed into cages, plasma levels of PRL significantly decreased and were maintained at low levels in both groups. The concentration of LH did not change in either group during the two wk after surgery when the hens were incubating eggs. After the hens were placed into cages, the concentration of LH increased in the OVX hens and was maintained at significantly higher levels than in the sham-operated hens. By contrast, the concentration of LH increased within 4 days after OVX of out-of-lay but nonincubating hens. The delay in the postcastration increase in plasma level of LH in the OVX hens was not associated with anorexia of incubating hens, since plasma levels of LH were not affected by force-feeding unless plasma levels of PRI were suppressed by nest deprivation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of a long-acting LHRH agonist preparation on plasma gonadotropin and prolactin levels in castrated male rats and on the release of prolactin from ectopic pituitaries

We have examined the effects of a single subcutaneous injection of an LHRH agonist, D-Trp-6-LHRH, in biodegradable microcapsules of poly(DL-lactide-co-glycolide) on plasma gonadotropin and prolactin (PRL) levels in castrated and in castrated-hypophysectomized-pituitary grafted (CAST-APX-GRAFT) male rats. The results were compared to the effects of daily injections of the same LHRH agonist dissolved in saline. In castrated rats, there were no significant alterations in plasma LH or PRL levels during the 10 days following the injection of LHRH agonist microcapsules, while FSH levels were generally reduced. In castrated males given daily injections of 6 micrograms of LHRH agonist in saline, plasma LH levels were significantly reduced while plasma PRL levels were not changed. In CAST-APX-GRAFT rats, both D-Trp-6-LHRH microcapsules and daily LHRH agonist injections appeared to increase plasma PRL levels. The pattern of changes in PRL release in both groups was similar, with levels on day 6 being significantly higher than those measured on days 1, 3 and 10 after onset of treatment. As expected, LH and FSH levels in these animals were extremely low. Immunoreactive D-Trp-6-LHRH was consistently detectable in the plasma of CAST-APX-GRAFT animals after microcapsule administration, whereas in animals given daily injections of this agonist in saline, its plasma concentrations were often below the detectability limit of the employed assay. These findings suggest that the LHRH agonist, D-Trp-6-LHRH, is capable of causing a short term stimulation of PRL release from ectopic pituitaries. Elevation of plasma LH levels is apparently not required for this effect.     

The effects of naltrexone, an opioid receptor antagonist, on plasma LH levels in common carp (Cyprinus carpio L.)

Naltrexone-an opioid receptor antagonist, was administered intraperitoneally to sexually mature male and female common carp in the prespawning period, in order to investigate its effects on spontaneous or sGnRH-A-stimulated LH secretion. Naltrexone and sGnRH-A were injected at the same time. The possible involvement of a dopaminergic system in this process was studied in males pre-treated with pimozide (a dopamine receptor antagonist) 12 h before naltrexone and/or sGnRH-A administration. Blood samples for the analysis of carp LH concentrations were taken just before the injections and then after the injections, serial sampling during 24 h was performed. In male carp, naltrexone (500 or 5000 microg kg(-1)) decreased spontaneous LH release, but there were no effects of naltrexone on sGnRH-A-stimulated LH secretion. In males pre-treated with pimozide, a similar response to naltrexone injection (500 microg kg(-1)) as in pirnozide non-treated fish, was observed. The highest dose of naltrexone, 5000 microg kg(-1), significantly stimulated LH release, in response to sGnRH-A administration in pimozide pre-treated males. In female carp, contrary to males, naltrexone at a dose of 500 microg kg(-1), caused significant stimulation of spontaneous LH release. These data indicate that endogenous opioid peptides modify LH secretion in sexually mature carp. In males, they stimulate LH secretion, acting rather on the hypothalamic GnRH system and in females, opioids inhibit LH release by the influence on the dopaminergic system.     

Face cooling-induced reduction of plasma prolactin response to exercise as part of an integrated response to thermal stress

This study was designed to verify if the decrease in blood prolactin (PRL) induced by selective face cooling during exercise could be part of a response to specific body thermal stress. Five healthy trained male cyclists presenting a significant plasma PRL elevation to exercise were, on three occasions and at weekly interval, submitted to a submaximal exercise (approx. 65% VO2max) on ergocycle with and without selective face cooling. In absence of face cooling a first trial served to establish reference values for workload, heart rate and plasma PRL levels, the latter increasing markedly (450% of resting values) in these conditions. On a second trial but with workload maintained at reference values (222 +/- 9 W), a significant bradycardia was observed with face cooling; furthermore, plasma PRL response to exercise was significantly reduced (to 31% of original response). On a third trial with face cooling, workload had to be significantly augmented (242 +/- 10 W) to maintain heart rate at reference level (78% HRmax); in addition, plasma PRL response to exercise was almost unchanged compared to the reference-value level. The absence of a significant face cooling-induced decrease in sympathetic tonus, as evaluated through peripheral plasma catecholamines response, does not indicate a role for the autonomic nervous system in the face cooling-induced reduction of both heart rate and PRL responses during exercise. Assay of circulating peripheral beta-endorphins could indicate that the face cooling-induced PRL blunted response does not necessarily involve an opioid mediation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Characteristics of flutamide action on prostatic and testicular functions in the rat

The effect of daily treatment with the pure antiandrogen Flutamide has been studied either alone or in combination with the LHRH agonist [D-Trp6, des-Gly-NH2(10)]LHRH ethylamide (LHRH-A), on testicular and prostatic functions in adult male rats. Treatment for 10 days with Flutamide (5 mg/rat, twice daily) caused a marked stimulation of plasma testosterone (T) associated with a significant increase in plasma gonadotropin concentrations and inhibited plasma PRL levels. Testicular weight is not changed following antiandrogen administration but testicular LH/hCG receptor levels are markedly decreased with no change in FSH receptor levels. Moreover, Flutamide treatment alone produces an important inhibition of ventral prostate and seminal vesicle weights associated with a significant decrease in prostatic beta-adrenergic receptor levels but no change is observed in specific ornithine decarboxylase (ODC) activity. Daily LHRH-A treatment at the dose of 1 microgram/day for 10 days decreases plasma T to levels comparable to those found in orchiectomized men (0.30 +/- 0.5 ng/ml). This effect is associated with an almost complete loss of testicular LH/hCG receptors, a decrease in testicular weight, a significant increase in plasma gonadotropins and a marked inhibition of plasma PRL concentration. A relatively smaller inhibition of ventral prostate and seminal vesicle weights follows treatment with the LHRH agonist alone, this effect being accompanied by a significant reduction in beta-adrenergic receptor concentration but no change in prostatic ODC activity. Combination of the two drugs, however, caused a potent inhibitory effect on both ventral prostate and seminal vesicle weight to values similar to those found in castrated rats. The prostatic weight loss is accompanied by a marked fall in ODC activity and in the concentration of beta-adrenergic receptors. The present data clearly show that combined treatment with an LHRH agonist and a pure antiandrogen is highly effective in inhibiting, not only prostatic growth, but also two androgen-sensitive parameters of prostatic activity.     

Effects of dopamine receptor stimulation on opiate-induced modifications of pituitary-gonadal function

We evaluated the effects of the dopaminergic drug bromocriptine (Br) on prolactin (PRL), luteinizing hormone (LH) and testosterone (Te) levels in a homogeneous group of opiate addicts in a methadone maintenance program (20 mg twice daily). Basal blood levels of PRL, LH and Te were determined in 15 adult male drug addicts, before 30 and 60 days after Br administration (7.5 mg/day) was started. 15 healthy volunteers served as controls for the evaluation of basal values of the hormones. Before treatment PRL values were high, while LH and Te levels were lower than normal. 30 days later, PRL lowered significantly while LH and Te increased significantly. 60 days later, the blood hormone values were still significantly different from pretreatment values, and close to the normal range. This observation shows that Br, probably through an increase of dopaminergic tone, may counteract some effects of opiates on the hypothalamic-pituitary-gonadal axis.     

Naloxone injected into the preoptic region has hypophysiotropic and seizurogenic actions in rats.

The effects of microinjection of naloxone, an opiate receptor antagonist, into the medial preoptic area (MPO) and diagonal band of Broca (DBB) on luteinizing hormone (LH) and prolactin (PRL) secretion were examined in the intact male rat and female rat in diestrus 1. In both the male and female rats, the injection of 50 micrograms naloxone at 1300 h produced an acute, two- to three-fold increase in serum LH, attaining the peak at 20 min. The PRL concentration in the female 20 min-2 h after the injection was significantly lower than in the saline-injected rat. In the male rat, naloxone caused a decrease in the PRL concentration in the late afternoon when a small rise occurred in the saline-injected rat, although it caused no immediate changes. In addition to these hypophysiotropic effects, naloxone injected in the MPO and DBB unexpectedly had seizurogenic actions. More than 40% of the animals of both sexes given an injection of naloxone had behavioral seizures, which began after about 20 min and were repeated intermittently at 15-20 min intervals through the sampling period of 6 h. In the LH and PRL response to naloxone, there was no significant difference between animals with and without seizure response in both sexes. The results suggest that in the preoptic opioid system there is no difference according to sex in the control of LH, and only a small one, if any, in the control of PRL. Further, on the basis of previous reports, there is a GABAergic system in the preoptic region, that is antagonized by naloxone and causes the activation of cortical neuronal activity.     

Possible involvement of endogenous opioid peptides in prolactin secretion induced by alpha 2-adrenergic stimulation in rats

Noradrenergic mechanisms have a stimulatory role in regulating prolactin (PRL) secretion in the rat. We investigated the mechanism by which the alpha 2-adrenergic system stimulates PRL release in urethane-anesthetized male rats. Intracerebroventricular injection of norepinephrine (2 micrograms/rat) or epinephrine (100 ng and 1 microgram/rat) caused an increase in plasma PRL levels. The PRL increase induced by epinephrine was much greater than that by norepinephrine. Intracerebroventricular injection of phentolamine (1 microgram/rat), an alpha-antagonist, blunted the plasma PRL increase induced by epinephrine (100 ng intracerebroventricularly). Plasma PRL levels were increased by intravenous injection of alpha 2-agonists, clonidine (15 micrograms/100 g of body wt), and xylazine (200 micrograms/100 g of body wt). Plasma PRL increase induced by clonidine or xylazine was suppressed by intravenous injection of naloxone (125 micrograms/100 g of body wt), an opiate antagonist. These findings suggest that alpha 2-adrenergic mechanisms stimulate pituitary PRL secretion, at least partly, by activating endogenous opioid peptides in the rat.     

Effects of sequential acute stress exposure on stress-induced pituitary luteinizing hormone and prolactin secretion

The present study was carried out to determine the effects of repetitive acute stress exposure on pituitary secretion of both luteinizing hormone (LH) and prolactin (PRL). Adult male rats were exposed to sequential episodes of acute novel environment stress separated by intervals of either 60 or 120 minutes. Serial blood samples were obtained from animals before, during and after each stress episode via indwelling intra-cardiac cannulas. The imposition of 10 minute episodes of novel environment stress on an hourly basis eventually rendered the hypothalamic-hypophyseal LH axis refractory to the stimulatory effect of stress. If sequential stress was imposed at 120 minute intervals, LH release was significantly enhanced during each exposure. A different pattern of PRL release was observed during the same sequential stress schedule. After an initial increase in hormone release in response to the first hourly stress episode, PRL levels were unaltered during the second and third hourly stress exposures. Thereafter, plasma PRL levels showed a trend toward a progressive increase in release during each successive episode, and were significantly elevated above preceding baseline levels during the fourth and fifth hourly stress exposures. In rats exposed to stress every two hours, a significant increase in PRL levels occurred following the first, but not the second stress episode. Hormone release was again enhanced in response to the third exposure to novel environment. The present results demonstrate that the repetitive exposure to acute novel environment stress results in differential alterations in pituitary LH and PRL secretion over time, and that the timing of repeated episodes is an important determinant of continued responsiveness to stress, particularly with regard to LH release. These findings suggest that the LH and PRL hormonal responses to at least this specific stressor are mediated by independent neural mechanisms.     

Preovulatory secretion of progesterone, luteinizing hormone, and prolactin in 4-day and 5-day cycling rats

Timing of ovulation and changes in plasma progesterone, luteinizing hormone (LH), and prolactin (PRL) during periovulatory stages were determined in Holtzman rats exhibiting regular 4- or 5-day cycles under a daily artificial illumination from 0500 to 1900 h. The 5-day cycling rats ovulated between 0130 and 0930 h on estrus, whereas some of the 4-day cycling animals ovulated as early as about 0130 h and others as late as 1130 h on estrus. Onset time of preovulatory LH and progesterone surges was about 1500 h on proestrus in both the 4- and the 5-day cycling rats. Peak levels of plasma LH and progesterone were measured at 1700 to 1900 h on proestrus, while the first rises and peak values of plasma PRL were evident a few hours earlier than those of plasma LH in the rats with two cycle lengths. Plasma LH levels at 1900 h on proestrus as well as plasma progesterone levels at 1600 and 2300 h on proestrus and at 0130 and 0330 h on estrus were significantly lower in the 5-day cycling rats than in the 4-day cycling animals (p less than 0.05). In contrast, PRL levels from 1500 through 2300 h on proestrus remained consistently higher in 5-day cycling rats than in 4-day cycling rats, and significant differences in PRL levels between these rats were apparent at 1500, 1600, and 2100 h (p less than 0.05-0.01). Thus, these results demonstrate that the 5-day cycling rats exhibit the attenuated magnitude of LH surge accompanied by the augmented preovulatory PRL release, and that plasma progesterone levels reflect the magnitude of LH surge. A tentative working hypothesis concerning the etiology of the 5-day cycle has been proposed.     

Serum and semen levels of immunoreactive prolactin, LH and FSH in normospermic, oligospermic and azoospermic men with obstructive infertility prior to and after vasoepididymostomy.

Attempts were made to validate RIA for prolactin (PRL), LH and FSH in semen from normospermic, oligospermic and azoospermic subjects. The RIA used to measure PRL and LH in semen fulfilled the criteria of reliability, whereas low levels of FSH in semen precluded the validation of FSH assay in semen. Semen levels of PRL and LH were significantly (P < 0.05) higher than serum levels in all groups of subjects investigated. Semen levels of FSH in azoospermic men after vasoepididymostomy (VEA), were significantly (P < 0.05) higher compared to azoospermic men prior to surgery. Serum levels of PRL were significantly higher (P < 0.05) in normospermic men compared to oligospermic and azoospermic men prior to and after surgery. Semen levels of PRL in normospermic men were comparable with oligospermic and azoospermic subjects prior to and after surgery. Serum levels of LH in oligospermic and azoospermic men who did not undergo surgery and in men reporting oligospermia after VEA were comparable to normospermic subjects but in men showing azoospermia post surgically, serum LH levels were significantly (P < 0.005) elevated. Semen levels of LH in men reporting azoospermia before surgery and in subjects showing oligospermia or azoospermia post surgically were significantly lower (P < 0.05) compared to men with normal sperm count. Serum levels of FSH were significantly elevated (P < 0.05) compared to semen levels in oligospermic men prior to surgery but this increase was not seen in post VEA subjects. These results were discussed.     

Prolactin levels in the western spotted skunk: changes during pre- and periimplantation and effects of melatonin and lesions to the anterior hypothalamus

Prolactin (PRL) is the primary pituitary hormone responsible for initiating increased function of the corpus luteum and blastocyst implantation in the western spotted skunk. Therefore, we have designed experiments to validate a PRL RIA, characterize the preimplantation profile in PRL secretion, and determine the effects of exogenous melatonin and lesions to the anterior hypothalamic area (AHA) on PRL secretion in the skunk. These objectives were investigated with a heterologous RIA using canine PRL standards and antiserum. Displacement curves of skunk pituitary extract and serum were parallel to the canine PRL standard curve. Growth hormone-releasing hormone injection did not cause a significant change in plasma PRL levels as detected by the assay (p = 0.74). Injection of pimozide increased and bromocriptine decreased plasma PRL levels (p less than 0.05). A seasonal trend in plasma PRL levels was observed during the preimplantation period, with mean concentrations ranging from 5 ng/ml during the period of short day length in January to 17.1 ng/ml during the long day photoperiod in early May. The average date of blastocyst implantation in this study was 2 May (n = 16). Silastic capsules containing melatonin (n = 5) significantly delayed both the seasonal rise in plasma PRL levels and the time of implantation (p less than 0.05) compared to controls with empty capsules (n = 4). Lesions to the AHA (AHAx, n = 5) eliminated these effects of melatonin on both the rise in PRL and time of implantation. PRL levels were highly correlated with progesterone levels (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Interactions of human growth hormone and prolactin on pituitary and Leydig cell function in adult transgenic mice expressing the human growth hormone gene

Adult male transgenic mice expressing the human growth hormone (hGH) gene are hypoprolactinemic. To evaluate the effects of exogenous prolactin (PRL) and endogenously secreted hGH on pituitary and Leydig cell function, adult male transgenic and nontransgenic mice (10-16 wk of age) were treated s.c. with either saline-polyvinylpyrrolidone (PVP) or oPRL (100 micrograms/mouse) in saline-PVP. Animals were treated twice daily; a total of 7 injections were given. One hour after the last injection, each group of mice was treated i.p. either with saline or oLH (0.3 microgram/g BW); 2 h later, blood was obtained via heart puncture. Plasma FSH, LH, PRL, androstenedione (A-dione), and testosterone (T) levels were measured by validated RIAs. Basal PRL levels were significantly lower (p less than 0.001) and basal LH concentrations were significantly higher (p less than 0.01) in transgenic than in nontransgenic mice. Administration of PRL significantly decreased (p less than 0.01) plasma LH levels in transgenic mice, whereas similar treatment of nontransgenic mice increased (p less than 0.01) circulating LH concentrations. Plasma FSH levels were unaffected in transgenic and nontransgenic mice treated with saline or PRL. Basal plasma A-dione and T levels were similar in both groups of animals and were significantly increased after treatment with LH. Administration of PRL increased T levels in transgenic and nontransgenic mice, but the T response to LH treatment was greater in PRL-treated transgenic mice, indicating the synergistic effect of hGH in the biosynthesis of T.(ABSTRACT TRUNCATED AT 250 WORDS)