Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PROLACTIN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,747 records · Page 97Linked to original sources

Studies on human sexual development. IV. Fetal pituitary and serum, and amniotic fluid concentrations of prolactin.

Prolactin concentrations were measured in 161 amniotic fluid specimens from 8-40 weeks fetal age and the levels compared with those observed in 45 fetal and neonatal cord sera and in 42 fetal pituitary specimens. Amniotic fluid prolactin levels rose steeply between 12-16 weeks gestation, and then declined to term; the calculated total amniotic fluid content of prolactin showed a similar pattern, but the peak was later, at about 26 weeks gestation. Amniotic fluid concentrations consistently exceeded fetal serum prolactin levels, even during the last trimester, when fetal serum and pituitary levels were highest. The data are compatible with a fetal origin for amniotic fluid prolactin, but only if one assumes that flux of prolactin out of amniotic fluid compartment is negligible, that the fetal kidney in mid-pregnancy clears prolactin at a rate virtually equal to the glomerular filtration rate, and the fetal pituitary shows secretion characteristics quite different from those of the adult gland.

Amniotic Fluid↗

Diminished prolactin reserve: a case report.

A 17 year old male patient presented with short stature and delayed puberty. Investigations showed normal thyroid function and intact TSH response to TSH-releasing hormone (TRH). Although basal levels of LH were low, both LH and FSH rose following the administration of LH-releasing hormone (LHRH). ACTH secretion assessed indirectly by the cortisol response to insulin hypoglycemia was normal. Growth hormone levels increased following the onset of sleep, as well as after the administration of insulin, L-dopa and L-arginine. Basal levels of prolactin were low (2-5 ng/ml) compared with 5-12 ng/ml in controls. There was a markedly impaired prolactin response to TRH (maximum rise above basal values of 3 ng/ml compared to a rise of 12-29 ng/ml in controls). Prolactin levels did not rise after the administration of chlorpromazine or L-arginine. There was some suppression of prolactin levels after L-dopa. Similar patterns of prolactin are seen in panhypopituitarism, where they are usually associated with other hypophyseal hormonal deficiencies. The diminished prolactin reserve demonstrated in this subject in the presence of intact function of the remainder of the anterior pituitary is compatible with the diagnosis of diminished prolactin reserve.

Adolescent↗

Use of serum prolactin in diagnosing epileptic seizures: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.

OBJECTIVE: The purpose of this article is to review the use of serum prolactin assay in epileptic seizure diagnosis. METHODS: The authors identified relevant studies in multiple databases and reference lists. Studies that met inclusion criteria were summarized and rated for quality of evidence, and the results were analyzed and pooled where appropriate. RESULTS: Most studies used a serum prolactin of at least twice baseline value as abnormal. For the differentiation of epileptic seizures from psychogenic nonepileptic seizures, one Class I and seven Class II studies showed that elevated serum prolactin was highly predictive of either generalized tonic-clonic or complex partial seizures. Pooled sensitivity was higher for generalized tonic-clonic seizures (60.0%) than for complex partial seizures (46.1%), while the pooled specificity was similar for both (approximately 96%). Data were insufficient to establish validity for simple partial seizures. Two Class II studies were consistent in showing prolactin elevation after tilt-test-induced syncope. Inconclusive data exist regarding the value of serum prolactin following status epilepticus, repetitive seizures, and neonatal seizures. RECOMMENDATIONS: Elevated serum prolactin assay, when measured in the appropriate clinical setting at 10 to 20 minutes after a suspected event, is a useful adjunct for the differentiation of generalized tonic-clonic or complex partial seizure from psychogenic nonepileptic seizure among adults and older children (Level B). Serum prolactin assay does not distinguish epileptic seizures from syncope (Level B). The use of serum PRL assay has not been established in the evaluation of status epilepticus, repetitive seizures, and neonatal seizures (Level U).

Diagnosis, Differential↗

Prolactin secretion following repetitive seizures.

We studied serum prolactin levels after 24 seizures occurring in eight subjects. Video-EEG intracranial monitoring confirmed temporal or frontal partial seizures. Seizure type, focus, and duration were similar for seizures with and without significant postictal prolactin elevations. The seizure-free interval (the time between seizures) varied considerably. Seizures occurring after longer seizure-free intervals (31.75 to 240 hours) showed robust prolactin responses. After shorter seizure-free intervals (1.07 to 25.42 hours), prolactin responses were reduced. This suggests that the amount of releasable prolactin is limited, depleted by seizures, or perhaps inhibited by prolactin feedback. Seizure-free intervals should be considered when interpreting prolactin levels.

Adult↗

Factors in predicting outcome from operation in patients with prolactin-secreting pituitary adenomas.

Forty female patients with pituitary adenomas were studied retrospectively to determine whether factors could be identified that would help predict outcome from operation. Twenty-five patients had a normal prolactin level (less than or equal to 30 ng/ml) during the early postoperative period (less than or equal to 3 months) and 15 patients had persistent disease (prolactin greater than 30 ng/ml). Nine of the 25 patients who initially had normal prolactin levels during the early postoperative period were found to have elevated prolactin levels during the late postoperative period (greater than 3 months). As has been shown previously, tumor size and preoperative prolactin levels were important factors in predicting surgical outcome. Patients with smaller (Hardy Grades I and II) tumors had significantly better outcome than those with larger (Hardy Grades III and IV) tumors. Patients with successful surgical outcomes had significantly lower preoperative prolactin values (204 ng/ml) than those with operative failures (524 ng/ml). In addition to the known factors, the patient's age at the time of operation, the length of amenorrhea, and the patient's growth hormone response to insulin hypoglycemia were newly identified as factors that helped predict surgical outcome. Patients who were less than or equal to 26 years of age and who had had amenorrhea for less than or equal to 6 years at the time of operation had significantly better surgical outcomes. Patients with normal growth hormone responses to stimulation testing had significantly better surgical outcomes than those with a blunted preoperative growth hormone response. The data suggest that prolactin-secreting pituitary tumors may cause a progressive disorder for which operative cure may be obtained only early in the disease.

Adenoma↗

Decreased expression of fos-related antigens (FRAs) in the hypothalamic dopaminergic neurons after immunoneutralization of endogenous prolactin.

In our previous studies we found that administration of exogenous prolactin increased dopamine turnover in the terminal areas of the hypothalamic dopaminergic neurons controlling prolactin secretion from pituitary lactotrophs. In this study we investigated the effect of immunoneutralization of endogenous prolactin on the expression of FRAs in the tuberoinfundibular dopaminergic (TIDA), tuberohypophysial dopaminergic (THDA), and periventricular hypothalamic dopaminergic (PHDA) subpopulations of the hypothalamic dopaminergic neurons. Female rats were ovariectomized on d 0 of the experiment. At 1000 h of d 10, all animals were injected with 20 microg of 17-beta-estradiol sc to induce a proestrous-like surge of prolactin at 1700 h the next day. At 1000 h on d 11, half of the animals were injected with 200 microL of rabbit anti-rat prolactin antiserum ip, while the controls received normal rabbit serum. Groups of animals were sacrificed for immunocytochemistry in 2 h intervals between 1300 and 2100 h. Double-label immunocytochemistry for FRAs and tyrosine hydroxylase (TH) was performed and the results are presented as percentage of TH-immunoreactive neurons expressing FRAs. In the control animals, expression of FRAs decreased at 1500 h, gradually increased by 1900 h, but was lower than the basal levels by 2100 h. Expression of FRAs was significantly lower at 1900 h in the PHDA, THDA and TIDA neurons of prolactin antiserum treated rats than in the controls. These results indicate that elimination of endogenous prolactin from the circulation lowers the activity and/or prevents the reactivation of neuroendocrine dopaminergic neurons at the beginning of the dark phase.

Animals↗

Binding of mouse choriomammotropin to prolactin receptors in the mouse mammary gland.

The interaction between mouse choriomammotropin and mouse mammary glands was examined by radioreceptor assays using ovine prolactin (NIH-P-S9) iodinated by lactoperoxidase as a tracer. Mouse pituitary extracts and placental extracts were subjected to 10% acrylamide gel electrophoresis. Gels were cut into 2-mm segments after electrophoresis, and stored in 1 ml 0.05 M phosphate buffer (pH 7.4) containing 0.05 M NaCl overnight for elution. Lactating mammary tissues from D strain mice were incubated for 120 min in 1 ml Medium 199 containing 6 ng of 125I-prolactin and 0.1 ml of each eluate. Pituitary extracts displaced 125I-prolactin only at the position which coincides with the prolactin band. Displacement was observed at two positions of the gel when placental extracts were used. Relative mobilities (Rm) were 0.21 and 0.71, respectively. The slowly migrating component of choriomammotropin inhibited the binding of 125-I-prolactin more strongly that the rapidly migrating one. Neither of them was identified as a distinct band in stained gels. The molecular weight of ovine prolactin, mouse pituitary prolactin and the slowly migrating component of mouse choriomammotropin was estimated to be 23000 using disc electrophoresis but the ion charges of these hormones were considerably different.

Animals↗

Effect of sulpiride on serum growth hormone and prolactin concentrations following L-DOPA administration in man.

The effect of chronic administration of sulpiride on serum human growth hormone (hGH), prolactin and thyroid stimulating hormone (TSH) was examined in 6 normal subjects. Sulpiride was given orally at a dose of 300 mg (t.i.d.) for 30 days. Sulpiride raised serum prolactin levels in all subjects examined. In addition, sulpiride suppressed hGH release induced by L-dopa, although the basal hGH level was not changed. Sulpiride treatment appeared to antagonize partially the inhibitory effect of L-dopa on prolactin release. Following thyrotropin-releasing hormone (TRH) injection, the percent increment in prolactin levels from the baseline in sulpiride-treated subjects was less than in controls without sulpiride. In contrast, both the basal and TRH-stimulated TSH levels were not influenced by sulpiride. These observations suggest that sulpiride suppresses L-dopa-induced hGH release and stimulates prolactin release, presumably by acting against the dopaminergic mechanism either on the hypothalamus or on the pituitary. The decreased prolactin response to TRH after sulpiride treatment may indicate a diminished reserve capacity in pituitary prolactin release.

Administration, Oral↗

Pulsatile secretion of prolactin and oxytocin during nursing in the lactating rat.

The secretory profile of prolactin and oxytocin in response to suckling stimuli by litters was studied in unanesthetized and urethane-anesthetized lactating rats. Serum prolactin levels were determined by radioimmunoassay. Oxytocin released at milk-ejection reflex was monitored by the changes in the intramammary pressure and/or the characteristic pup's reaction associated with the milk ejection. Serum prolactin concentrations began to rise earlier than the first milk ejection in unanesthetized rats, but they were never elevated without the appearance of milk ejections in urethane-anesthetized rats. Pulsatile fluctuation in serum prolactin levels at 6-15 min intervals was observed in the nursing period when 10 pups were suckling continually. The intermittent milk-ejection reflex occurred not always but preponderantly (64-91%) when the serum prolactin levels were at the nadir of the fluctuation. Injection of an estimated dose of oxytocin released at each milk ejection (1 mU) did not change the serum prolactin levels. These results indicate that the mechanism for prolactin release may be more susceptible to the effects of anesthesia than that for oxytocin release in response to the suckling stimuli and that the release of both the hormones is pulsatile in nature and be influenced by a common biological clock during the nursing period.

Animals↗

Prolactin does not mediate the suppressive effect of the suckling stimulus on luteinizing hormone secretion in ovariectomized lactating rats.

The plasma LH concentration in ovariectomized lactating rats is low for 14 days postpartum, while the prolactin concentration is high during this period. We examined the effect of the inhibition of increased prolactin secretion with bromocriptine (CB-154) on the LH secretion in lactating rats ovariectomized on day 2 (day 0 = day of parturition). Blood samples were collected through an indwelling atrial cannula every day. LH levels were kept low until day 9 in lactating rats injected daily with CB-154 (0.6 mg/day, s.c.). The duration of the period during which LH secretion was suppressed was shorter in lactating rats treated with CB-154 than in saline-injected controls. The replacement with ovine prolactin by means of a mini-osmotic pump (0.3 mg/day, s.c.) in CB-154-treated lactating rats restored the duration of LH suppression. In rats deprived of their pups on day 2, the LH concentration rose immediately after removal of the pups and the LH level was not significantly different between rats treated with CB-154, ovine prolactin and saline, indicating that neither the CB-154 treatment nor the high level of prolactin alone has any effect on LH secretion in rats deprived of their pups. The present results clearly demonstrate that prolactin does not mediate the suppressing effect of the suckling stimulus on LH secretion in early lactation and support our theory that the suckling stimulus controls the LH and prolactin secretion independently at the hypothalamic level.

Animals↗

Partial purification of prolactin-like substance from snake (Ptyas mucosa) pituitaries.

Pituitary extract of the common rat snake (Ptyas mucosa) was found to be capable of displacing the binding of 125I-labelled ovine prolactin to female rat liver membranes, suggesting the presence of prolactin-like substance in snake pituitary. The snake prolactin-like substance was unadsorbed on Concanavalin A-Sepharose, but adsorbed on DEAE-cellulose. The partially purified snake prolactin-like substance was also capable of displacing the binding of 125I-labelled ovine prolactin to snake kidney and large intestine membranes. Chromatographic fractions derived from snake pituitary and which possessed potent growth hormone receptor binding activity were devoid of prolactin receptor binding activity, suggesting the existence of distinct prolactin-like and growth hormone-like substances in snake pituitary.

Animals↗

The glycosylation as source of the variability in prolactin patterns of individual human amniotic fluids.

Whilst it is known that prolactin has size heterogeneity in human amniotic fluid, no studies exist concerning the heterogeneity between individual amniotic fluids and the molecular properties of the prolactin forms which are connected with such a variability. To elecit this, prolactin forms from amniotic fluid taken from 6 full-term deliveries and processed separately, were fractionated by ConA-Sepharose, and characterized by SDS-PAGE, immunoblotting, and glycan detection of blotted prolactins. Recording the absorbance at 280 nm, dimers in the wash of the ConA-Sepharose column and in the elution with methyl-alpha-D-glucoside were evident in 3 fluids. The proteins of the chromatographically more rapid and retarded migrating fractions, generating the first dimer, of unbound material consisted on average of 74-83% and 85-90% of prolactin forms. The eluted fractions (bound material) contained 10-27% of the prolactin amount of the unbound fractions. The electropherograms using 12.5% gels indicated identical patterns of bands in repeated experiments per fluid but variability between the charges. Thus, the apparent molecular masses (kDa) and the proportions to the total prolactin (%) were 14.5-16 (8-12%), 20-23 (3-5%), 24 (4-8%), 25 (6-10%), 27 (19-25%), 28-29 (6-9%), 39-43 (0.5-1.0%), 60-64 (12-19%), 87-90 (8-11%) and 117-140 (2-7%) in nonreducing electrophoretical conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗

The relationship of prolactin in cord blood, gestational age and respiratory compliance after birth in newborn infants.

In 29 healthy newborns (gestational age 30-41 weeks) and 7 newborns with respiratory distress syndrome (gestational age 28-31 weeks) the prolactin levels in the cord blood and respiratory compliance was measured. Prolactin was determined by radioimmunoassay, the respiratory compliance was measured with the airway occlusion technique in spontaneously breathing newborns and with injection of known volumes and measuring the airway pressure in newborns with ventilatory support. In healthy newborns prolactin and gestational age were significantly correlated (r = 0.62, p less than 0.001), while prolactin did not correlate with respiratory compliance (r = 0.22, n. s.). Comparing 5 healthy newborns and the 7 RDS infants with prolactin values below 170 ng/ml, there was no significant difference in the prolactin levels, but in the compliance values. We conclude that prolactin does not directly influence lung maturation, but is associated with gestational age.

Fetal Blood↗

Increased serum prolactin in diabetic ketoacidosis; correlation between serum sodium and serum prolacting concentration.

In 8 patients with diabetic ketoacidosis, serum prolactin was measured and found to be elevated (24.8 +/- 10.2 ng/ml, mean +/- SEM). After correction of the ketoacidosis, the prolactin level decreased to 10.9 +/- 6.4 ng/ml (normal range men 4.9 +/-0.8, women 5.1 +/- 1.6 ng/ml). The scatter of prolactin values was wide. A study of the correlation between the serum prolactin values and chemical parameters that are altered in diabetic ketoacidosis was therefore undertaken. Serum prolactin values did not correlate well with the serum bicarbonate concentration or serum osmolality. However, a significant negative correlation between log serum prolactin concentration and serum sodium concentration was demonstrated (r = -0.61, P less than 0.01). It is suggested that serum prolactin may possible participate in sodium retention in man as has been demonstrated in studies on animals.

Adult↗

Homologous radioimmunoassay for canine prolactin.

A homologous double antibody radioimmunoassay has been developed for canine prolactin. Purified canine prolactin was iodinated by lactoperoxidase/H2O2 to an average of 101 "+/- 10.1 muCi/microgram. Antiserum was used at a final dilution of 1:80 000 and at this concentration bound approximately 20% of the added tracer in the absence of competing unlabelled prolactin. Partial cross-reaction was observed with ovine and bovine prolactin but there was no cross-reaction with a highly purified canine growth hormone preparation. Dilutions of pregnant and lactating bitch sera were parallel to the purified canine prolactin standard curve. Mean prolactin levels in normal male and anoestrous females were 8.8 +/- 0.8 and 12.6 +/- 2.6 ng/ml, respectively. Thyrotrophin-releasing hormone (TRH) induced a consistent elevation in prolactin levels 15--30 min after intravenous injection.

Animals↗

Influence of oestrogen administration in vivo and in vitro on the release and synthesis of prolactin from incubated pituitaries.

The release and synthesis of prolactin were studied in incubated adenohypophyses from ovariectomized rats. After a 4 h incubation period the prolactin concentration in the medium markedly increased whereas that in the gland was reduced. However, the concentration of prolactin in the system, tissue plus medium, after 4 h was almost twice as much as that present at the beginning of incubation indicating spontaneous synthesis. This spontaneous release and synthesis of prolactin was greatly increased in incubated glands from ovariectomized oestrogen-treated rats. Oestradiol benzoate was injected in doses of 2.5, 5.0 or 10.0 microgram/rat 2 or 24 h before killing the animals. Lower effects were obtained in glands from 2 h-oestradiol-pre-treated rats than from 24 h-oestradiol-primed rats. Oestradiol-17beta (55, 166, 500 and 1500 ng/ml) added to the incubation medium also enhanced the release and synthesis of prolactin and the effect was more marked in glands from oestrogen injected rats than in those of non-treated animals. The increase was dose-related although the higher doses were less effective. These results provide further evidence of the effect of oestrogen on the release and synthesis of prolactin by a direct action on the pituitary gland. They also show that oestradiol pre-treatment in vivo increase the response of the prolactin cells towards oestradiol in vitro.

Animals↗

Effects of medial hypothalamic deafferentation on prolactin secretion in pseudopregnant rats.

Frontal hypothalamic deafferentation (FHD), which disconnects the anterior hypothalamus from the preoptic area, stops the twice daily surges of prolactin secretion of pregnancy or pseudopregnancy in the rat, and causes rapid luteolysis. Medial hypothalamic deafferentation (MHD), which separates the anterior from the posterior half of the hypothalamus, does not interrupt pregnancy and causes a significant increase in the size of the corpora lutea. To see whether MHD induces an increase in the basal level of prolactin secretion and/or a change in the pattern of prolactin surges, pseudopregnant rats were subjected to MHD or a sham operation on day 3 (day 1 = day of oestrus) and their bloods assayed for prolactin on either day 5 or days 7--8. MHD caused a specific disappearance of the day-time prolactin surge and a diminution in the height of the night-time surge, but no change from the controls in the basal prolactin level. In spite of what thus appears to be a lesser secretion of prolactin than in the controls, the corpora lutea of the MHD rats were larger, and progesterone was secreted at a higher rate and for a longer time, than in the controls. The relation of these findings to the existence of a "surge centre" in the hypothalamus was discussed.

Afferent Pathways↗

Acute suppressive effect of ACTH-induced cortisol secretion on serum prolactin levels in healthy man.

The effect of ACTH on serum prolactin concentrations was studied in 6 healthy women in the follicular phase of the menstrual cycle, in 5 healthy men and in 6 patients (5 males, 1 female) with adrenocortical insufficiency. In healthy women prolactin levels decreased from basal, 14.4 +/- 2.1 (SEM) microgram/l to 9.4 +/- 0.9 microgram/l after 30 min and to 8.1 +/- 0.7 micrograms/l after 60 min of iv administration of synthetic ACTH1-24 (0.25 mg). Upon continuous infusion of ACTH1-24 (0.25 mg for 8 h) prolactin fell to 4.4 +/- 0.6 microgram/l in healthy women and to 4.6 +/- 1.5 micrograms/l (basal: 10.6 +/- 1.8 micrograms/l) in healthy men. In patients with adrenocortical insufficiency prolactin concentrations remained unchanged following an 8 h infusion of ACTH1-24 (before ACTH: 14.5 +/- 2.3 micrograms/l, after ACTH: 16.3 +/- 3.1 micrograms/l). After treatment with dexamethasone (2 mg/day for 3 days) however, prolactin concentrations were suppressed both in healthy women (-52 +/- 7%) and men (-25 +/- 11%) and in patients with adrenocortical insufficiency (-21 +/- 10%). Thus the effect of ACTH on prolactin appeared to be mediated via enhanced cortisol secretion. It is suggested that an acute increase in cortisol levels within the physiological range may modulate prolactin secretion.

Addison Disease↗