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PubMed1980

[Secretion of prolactin in healthy men and women of different age (author's transl)].

In 50 healthy women and 57 healthy men aged 20--80 years serum-prolactin-levels before and after intravenous injection of 200 micrograms TRH were measured and correlations with serum-triglycerid-, sodium-, basal TSH and serum insulin levels as well as sodium concentration of red blood cells, age, relativ body weight (Broca) and blood pressure were calculated. In men of different age no changes in basal serum-prolactin-levels can be detected. In 60--80 years old men a significant higher but later occuring TRH-induced prolactin secretion than in younger men can be found. 50--59 year old women have a significant higher prolactin secretion after TRH application than 20--29 year old females. Basal serum prolactin levels of women correlate negative significant with serum sodium levels and positive significant with the sodium concentration of red blood cells and basal TSH values. Relative prolactin out-put (prolactin-max--prolactin-basal) after TRH-application in women is found to correlate positiv significant with serum triglycerid levels. In men relative prolactin out-put following TRH-injection correlates negativ significant with basal serum insulin levels. This correlation diminishes when age and Broca are kept constant in the calculation.

Adult↗
PubMed1978

Plasma prolactin in essential and renovascular hypertension.

Plasma prolactin response to postural change and variation in dietary sodium was evaluated in five normal volunteers and 15 patients with essential hypertension. Values at 0800 hours (11.9 +/- 3.5 ng/ml, mean +/- 1 S.D.) were uninfluenced by the duration of recumbency (10 or 34 hr) and were significantly higher than those obtained at noon (6.9 +/- 3.5 ng/ml, mean +/- 1 S.D., p less than 0.001). The latter were uninfluenced by postural change. There was no correlation between sodium intake and plasma prolactin, nor was there any apparent correlation between prolactin and plasma renin activity. There was no significant difference in prolactin concentrations between normotensive and hypertensive subjects. In 10 additional patients with unilateral renal disease, renal vein prolactin concentrations did not differ significantly from simultaneously obtained peripheral concentrations. Renal vein prolactin was uninfluenced by the presence of renal disease and did not correlate with renal blood flow. It is concluded that there is no evidence of feedback between sodium intake and prolactin in man. Human kidneys do not seem to clear significant amounts of prolactin. It appears unlikely that alterations in prolactin concentration, at least as assessed by daytime values, participate in the maintenance of either essential or renovascular hypertension. Since values at 0800 hours are frequently elevated as a reflection of preceding sleep-related peaks, sampling at 1200 hours may be preferable when search is undertaken for hypothalamic-pituitary disease.

Adult↗
PubMed1984

Effect of sultopride on prolactin secretion in rats.

Oral administration of sultopride caused a significant and dose-related increase in serum prolactin levels in the rat. Sultopride was 4-6 times as potent as sulpiride in stimulating prolactin secretion. Both drugs produced much greater stimulations of prolactin release in female rats than in male rats, suggesting the sex difference in response to drugs. CB-154, a dopamine agonist, inhibited the sultopride-induced prolactin release. Stereoselective activity of sultopride-isomers was observed in increasing rat prolactin secretion. Sultopride had no significant effects on LH and FSH basal levels in female rats. In a successive study, basal prolactin levels in the male rat were higher at 2-3 days, but lower at 6 and 14 days. Prolactin response 1 hr after sultopride administration was observed throughout the experiments. Sultopride neutralized the dopamine-mediated inhibition of prolactin secretion from the anterior pituitary in vitro. These results suggest that sultopride, like sulpiride, stimulates prolactin secretion by blocking the dopamine receptor in the pituitary.

Amisulpride↗
PubMed1984

Prolactin, aggression and hostility: a discussion of recent studies.

Several studies are summarized in which the relationship of high prolactin levels and self-rated anger-hostility was examined. The Symptom Questionnaire, a state measure which contains an anger-hostility scale, was included in all studies. Women with hyperprolactinemic amenorrhea were found to have higher hostility scores than amenorrheic women with normal prolactin levels. In another study, hyperprolactinemic women were found to have higher hostility scores than female family practice patients, random employees and there was a nonsignificant trend for higher hostility scores than in female nonpsychotic psychiatric outpatients. In both studies, depression and anxiety were also significantly higher. When bromocriptine, a prolactin lowering drug, was administered to hyperprolactinemic women in a double blind crossover study, there was a significant and progressive decrease of hostility, depression and anxiety while on bromocriptine, parallel with the decrease in prolactin and no change on placebo. Post-partum women who had high prolactin levels were significantly more hostile than a control group of employees and as hostile as hyperprolactinemic women. Hyperprolactinemic males were no more hostile than controls. The relationship of prolactin to post-partum aggression in mammals is briefly reviewed. The findings are inconclusive; in the three species studied, postpartum aggression is perhaps enhanced, but does not depend on high prolactin levels. There are no studies on the relationship of prolactin levels and violence in women. Hostility associated with high prolactin levels in postpartum women is perhaps a phylogenetic remnant which may have had the evolutionary advantage of protecting the young.

Aggression↗
PubMed1981

Serum prolactin during pregnancy induced by pituitary gonadotrophins in a patient with post partum hypopituitarism (Sheehan syndrome).

With the purpose of investigating if placental prolactin production had an influence on maternal prolactin serum concentrations, this hormone was quantitated in serum of a women with partial Sheehan syndrome (deficient gonadotrophin and prolactin production). Her pregnancy was induced by pituitary gonadotrophins and the deficient prolactin pituitary reserve was shown by means of pituitary stimulation test with metoclopramide of pituitary stimulation test with metoclopramide and TRH. Quantitative analysis of prolactin was made by RIA utilizing the double antibody method. Serum prolactin concentrations remained persistently low during pregnancy with a minimal increase (1 - 16 ng/ml) at the end of pregnancy when comparing with concentrations observed in normal pregnant women (20 +/- 10 ng/ml at the beginning of pregnancy, and 250 +/- 150 ng/ml mean +/- 3 SD at the end). Prolactin concentration in the umbilical cord was found to be within normal values (252 ng/ml). Results obtained showed that fetal and placental prolactin does not pass on to the mother and confirm the idea that maternal serum prolactin during pregnancy is exclusively of a maternal pituitary origin.

Adult↗
PubMed1994

Effect of ergovaline, loline, and dopamine antagonists on rat pituitary cell prolactin release in vitro.

Cultured rat pituitary cells were studied to: determine the effects of ergovaline and loline on in vitro prolactin release; delineate the agonistic activity of these alkaloids at the D2 dopamine receptor, using 2 selective D2 dopamine receptor antagonists; and compare the efficacy of 2 dopamine receptor antagonists in reversing effects of the treatments on in vitro prolactin secretion. Ergovaline reduced in vitro prolactin release by at least 40% (P < 0.05) at concentrations of 10(-4), 10(-6), and 10(-8) M. However, loline reduced (P < 0.05) prolactin release only at the highest concentration, 10(-4) M. Two standard dopamine agonists, dopamine and alpha-ergocryptine, were used to verify that the inhibitory control mechanisms of in vitro prolactin release were intact. Both compounds reduced prolactin release by at least 40% for concentrations of 10(-4), 10(-6), or 10(-8) M. Selective D2 dopamine receptor antagonists (10(-6) M), domperidone and sulpiride, reversed (P < 0.05) the effect of loline on in vitro prolactin release. However, only domperidone (10(-6) M) was able to reverse (P < 0.05) the effect of ergovaline and only at the lowest ergovaline concentration (10(-8) M). Domperidone was more effective (P < 0.05) in reversing the prolactin-suppressing effect of alpha-ergocryptine than was sulpiride. The dose-response curve for domperidone (cubic fit, P < 0.0001) indicated a threshold concentration (10(-7) M) for reversal of alpha-ergocryptine's (10(-8) M) effect on prolactin release. However, at similar concentration of sulpiride (quadratic fit, P < 0.007), a threshold level was not obtained.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaloids↗
PubMed1994

Tandospirone stimulates prolactin secretion in the rat by an action at serotonin-1A receptors.

Tandospirone is an azapirone drug that has high affinity for serotonin-1A (5-HT-1A) receptors and preclinical effects predictive of antidepressant and/or anxiolytic efficacy. 5-HT-1A receptor agonists, such as 8-hydroxy-2-(di-n-propyl-amino)tetralin, increase the plasma prolactin concentration in rats, probably by an action in the brain that leads to an increase in prolactin release from the pituitary gland. The purpose of this study was to examine the effect of tandospirone on plasma prolactin concentration in awake, freely moving male rats. We found that i.v. administration of tandospirone results in a rapid and dose-related increase in the plasma prolactin concentration. The plasma prolactin level peaks about 10 min after injection and returns to base-line values within 30 min after injection. The ED50 of tandospirone to increase plasma prolactin levels is approximately 0.3 mg/kg. This effect of tandospirone is blocked by pretreatment with the 5-HT antagonists metergoline and NAN-190 and shows cross-desensitization with the 5-HT-1A agonist 8-hydroxy-2-(di-n-propyl-amino)tetralin. Thus the effect of tandospirone on plasma prolactin concentration appears to be mediated by 5-HT-1A receptors. In contrast to this effect of tandospirone, 1-(2-pyrimidyl)-piperazine (1-PP), the common metabolite of tandospirone and other azapirone drugs, has no effect on plasma prolactin levels. The effect of chronic administration of tandospirone was examined by measuring the prolactin response to an acute i.v. injection of tandospirone 24 hr after the last of chronic injections of tandospirone (10 mg/kg, s.c., twice a day for 2 weeks).(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

[Effects of opiate receptor blockade with naloxone on prolactin (PRL) secretion in patients with diabetes type I (IDDM) with chronic renal failure treated with hemodialysis (HD)].

The aim of the study was to answer the questions: 1) does the prolactin secretion in the TRH test (0.4 mg i.v.) differ in haemodialyzed patients with diabetes nephropathy in the end stage renal failure in comparison to haemodialyzed chronic renal failure patients with non-diabetic nephropathy and healthy subjects; 2) does the opiate receptors blockade with naloxone (2 mg i.v.) modify the prolactin secretion during the TRH test in those patients. 39 subjects were studied. The patients were divided into three groups: group I: 12 haemodialyzed patients with IDDM and diabetic nephropathy in the end stage renal failure, group II: 15 haemodialyzed chronic renal patients with non-diabetic nephropathy and the control group: 12 healthy persons. The basic prolactin secretion and area over basic value (AOBV) of the prolactin were estimated. Prolactin concentration was measured by LIA. 1) The basic prolactin secretion was significantly higher in the patients with chronic renal failure. 2) The basic prolactin secretion in IDDM patients with diabetic nephropathy in the end stage renal failure treated with haemodialysis was significantly lower than in haemodialyzed patients with chronic renal failure of non-diabetic etiology. 3) TRH and TRH with naloxone caused significant increase of prolactin secretion in all investigated groups, but the increase is significantly lower in chronic renal failure patients than in healthy subjects. 4) Naloxone decreases significantly the prolactin secretion during TRH test only in haemodialyzed patients with chronic renal failure of non-diabetic etiology.

Adult↗
PubMed1997

Plasma concentrations of prolactin in overtly pseudopregnant Afghan hounds and the effect of metergoline.

The effect of metergoline, a 5-hydroxytryptamine (serotonin) antagonist, on the plasma concentrations of prolactin in overtly pseudopregnant Afghan hounds and on the clinical symptoms of overt pseudopregnancy were studied. Plasma concentrations of prolactin and progesterone were determined in six Afghan hounds with signs of overt pseudopregnancy for 2-3 weeks and in three Afghan hounds that were not pseudopregnant at the time of blood sampling. In the overtly pseudopregnant bitches the plasma concentrations of prolactin before treatment (35.5 +/- 8.5 micrograms l-1) were significantly higher than the plasma concentrations of prolactin of the three bitches that were not pseudopregnant (6.3 +/- 0.5 micrograms l-1); the latter values were similar to those of non-pseudopregnant beagle bitches during the total luteal phase. The six pseudopregnant Afghan hounds were treated for 10 days with the antiserotoninergic drug metergoline. At 2 h after the onset of treatment with metergoline, the mean plasma concentration of prolactin had decreased to 10.8 +/- 2.9 micrograms l-1. The plasma concentrations of prolactin continued to decline to 5.4 +/- 1.0 micrograms l-1 at 4 h and to 1.0 +/- 0.1 microgram l-1 during treatment days 3-10. Signs of pseudopregnancy, such as swelling of the mammary glands and digging, decreased during the treatment period. The treatment was associated with mild behavioural side effects such as whimpering and aggressiveness. These side effects are probably not related to suppression of prolactin but are due to a direct effect on serotoninergic pathways in the brain. It is concluded that high plasma concentrations of prolactin are associated with the development and maintenance of pseudopregnancy. The serotonin antagonist metergoline strongly suppresses plasma concentrations of prolactin in pseudopregnant dogs and decreases the clinical signs of pseudopregnancy.

Animals↗
PubMed1976

Measurement of pituitary hormones: clinical applications. 5. Prolactin.

A sensitive and specific assay for human prolactin has been developed using human prolactin and antiserum distributed by the United States National Pituitary Agency. Plasma prolactin concentrations in control subjects ranged from 0-20 ng/ml. No sex difference in prolactin concentration was observed. A brisk increase in plasma prolactin levels occurred in normal subjects during the administration of chlorpromazine and thyroid stimulating hormone releasing factor (TRH). These stimulatory tests of prolactin release should therefore be useful in the assessment of hypothalamic pituitary function. Basal plasma prolactin values were raised in most patients who were being treated with phenothiazines and were helpful diagnostically in patients with amenorrhoea, galactorrhoea, hypogonadism, cranio-pharyngioma, "non-functioning" pituitary tumours and acromegaly. In many of these disorders a significant reduction in the plasma prolactin concentration was observed following oral administration of bromocriptine. Plasma prolactin determinations should be useful in evaluating the response to medical treatment or pituitary ablation.

Acromegaly↗
PubMed1998

Acute effects of prolactin on passive calcium absorption in the small intestine by in vivo perfusion technique.

The acute effect of intraperitoneally administered prolactin (0.2, 0.4, and 0.6 mg/kg body weight) on passive calcium transport in duodenum, proximal jejunum, and ileum of sexually mature female Wistar rats was investigated by using an in vivo perfusion technique. Test solution containing (in mM) NaCl, 100; KCl, 4.7; MgSO4, 1.2; CaCl2, 20; D-glucose, 11; sodium ferrocyanide (Na4Fe(CN)6), an index of net water transport, 20; and 0.7 microCi 45CaCl2 (1 Ci = 37 GBq) was perfused through the 10-cm intestinal loop for 60 min. Results showed that 0.4 mg prolactin/kg body weight significantly increased duodenal net Ca absorption (net Ca) from 23.81 +/- 1.84 to 30.56 +/- 1.57 mmol/g dry weight (p < 0.05) by stimulating the lumen to plasma calcium flux (CaL-P). The jejunum responded to 0.2, 0.4, and 0.6 mg prolactin/kg body weight by reversing from net Ca absorption of 18.60 +/- 1.70 mmol/g dry weight to net secretion of -3.30 +/- 1.56, -10.39 +/- 2.21, and -11.79 +/- 2.04 mmol/g dry weight (p < 0.01), respectively, as a result of a dose-dependent increase in plasma to lumen calcium flux (CaP-L). Calcium fluxes in the ileum on the other hand did not respond to prolactin. There was a close correlation between net water flux and net calcium flux in all three intestinal segments under basal condition regardless of the luminal sodium concentration. However, this correlation was lost after prolactin administration, which while having no effect on net water flux, altered the duodenal and jejunal calcium fluxes. By varying the luminal concentration of sodium, it was found that the stimulatory effect of 0.4 mg prolactin/kg body weight on the duodenal CaL-P was reduced when compared with control, i.e., 17.84 +/- 0.91 vs. 26.64 +/- 1.05 mmol/g dry weight at a sodium concentration of 180 mM, and 14.48 +/- 0.99 vs. 20.12 +/- 1.34 mmol/g dry weight at a sodium concentration of 140 mM. At a sodium concentration of 80 mM, the prolactin effect was absent. Since duodenal Na(+)-K+ ATPase activity was increased by prolactin from 3.77 +/- 0.16 to 4.95 +/- 0.30 mumol Pi.mg-1 protein.h-1 (p < 0.05), sodium dependency of the prolactin-enhanced lumen to plasma calcium flux may be related to both sodium-induced water flow and calcium-sodium exchange across the basolateral membrane. Thus, it was postulated that under basal condition, net calcium transport in the small intestine occurred with the sodium-induced water transport along the paracellular pathway. However, after prolactin administration, this association was lost. Prolactin-enhanced lumen to plasma calcium flux in the duodenum was sodium dependent and involved the Na(+)-K+ ATPase activity. In the proximal jejunum, prolactin stimulated plasma to lumen calcium flux, but the mechanism was not known.

Absorption↗
PubMed2005

Prolactin daily rhythm in suckling male rabbits.

BACKGROUND: This study describes the 24-h changes in plasma prolactin levels, and dopamine (DA), serotonin (5HT), gamma-aminobutyric acid (GABA) and taurine concentration in median eminence and adenohypophysis of newborn male rabbits. METHODS: Animals were kept under controlled light-dark cycles (LD 16:8, lights on at 08:00 h), housed in individual metal cages, and fed ad libitum with free access to tap water. On day 1 after parturition, litter size was standardized to 8-9 to assure similar lactation conditions during the experiment. Groups of 6-7 suckling male rabbits were killed by decapitation on day 11 of life at six different time points during a 24-h period. RESULTS: Plasma prolactin levels changed significantly throughout the day, showing a peak at the beginning of the active phase (at 01:00 h) and a second maximum during the first part of the resting phase (at 13:00 h). Median eminence DA concentration also changed significantly during the day, peaking at the same time intervals as plasma prolactin. A single maximum (at 13:00 h) was found for adenohypophysial DA concentration. Individual adenohypophysial DA concentrations correlated significantly with their respective plasma prolactin levels. A maximum in median eminence 5HT concentration occurred at 21:00 h whereas adenohypophysial 5HT peaked at 13:00 h. Median eminence 5HT concentration and circulating prolactin correlated inversely. In the median eminence, GABA concentration attained maximal values at 21:00 h, whereas it reached a maximum at 13:00 h in the pituitary gland. Median eminence GABA concentration correlated inversely with circulating prolactin. In the median eminence, taurine values varied in a bimodal way showing two maxima, at the second half of the rest span and of the activity phase, respectively. In the adenohypophysis, minimal taurine levels coincided with the major plasma prolactin peak (at 01:00 h). Circulating prolactin and adenohypophysial taurine levels correlated inversely. CONCLUSION: The correlations among the changes in the neurotransmitters analyzed and circulating prolactin levels explain the circadian secretory pattern of the hormone in newborn male rabbits.

Journal Article↗
PubMed2002

Detection of prolactin receptor mRNA in the corpus striatum and substantia nigra of the rat.

The observation of prolactin modulation of the nigrostriatal dopaminergic system suggests the expression of prolactin receptor in the corpus striatum or substantia nigra. The present study investigated expression of prolactin receptor mRNA in tissues microdissected from the corpus striatum and substantia nigra of the rat. By using reverse transcription PCR combined with Southern hybridization, the long form of prolactin receptor mRNA was detected in the substantia nigra, caudate putamen, globus pallidus, and ventral pallidum in ovariectomized rats, whereas the short form was not detectable in any of these areas. Estrogen had no effect on expression of the long-form mRNA in the substantia nigra and corpus striatum. By using the RNase protection assay, the expression of both short and long forms of prolactin receptor mRNA was observed in the corpus striatum in ovariectomized rats. Again, levels of expression were not significantly altered by estrogen treatment. Both forms of prolactin receptor mRNA were clearly expressed in the choroid plexus and were up-regulated by estrogen treatment. The expression of both forms of prolactin receptor mRNA in nigrostriatal areas may help to support the hypothesis that prolactin has direct actions on these brain regions.

Animals↗
PubMed1992

Identification of prolactin receptors in hepatic nuclei.

Prolactin is a trophic hormone which may act directly at the hepatocyte nucleus. In this study, specific prolactin binding sites were sought in purified rat liver nuclei. Saturable and specific, high affinity 125I-prolactin binding sites were demonstrated to be on or within the nucleus. Prolactin binding was competitively inhibited by rat and ovine prolactins but not by rat growth hormone. Using immunogold electron microscopy, we detected prolactin receptors throughout the nucleus, in association with heterochromatin. Furthermore, endogenous immunoreactive prolactin was demonstrated to be within hepatic nuclei. We conclude that rat liver nuclei possess prolactin binding sites which likely participate in hormone-directed growth processes.

Animals↗
PubMed1984

Uptake and processing of prolactin by alternative pathways in rat liver.

The uptake and subcellular processing of radiolabelled prolactin has been studied in male and female rats. Analytical subcellular fractionation of liver homogenates from rats injected with 125I-prolactin showed that in female rats the prolactin was primarily internalised to low density (1.12 g X cm-3) membranes. Approx. 10-15% of the total label was found in high density membranes, similar in distribution to lysosomal marker enzymes. In the normal male rat, prolactin was internalised solely to lysosomal type membranes. However, in male rats treated with estrogen, the distribution of prolactin was very similar to that seem in the female, indicating that internalisation to low density membrane is dependent on the presence of prolactin receptors. Gel exclusion chromatography showed that the prolactin internalised to the lysosomal membranes was extensively degraded whereas that associated with the low density membrane remained intact. Use of digitonin, to establish the identity of the low density membrane gave inconclusive results, but suggested that the prolactin was associated with membrane bearing NADH pyrophosphatase rather than the classical Golgi marker, galactosyltransferase.

Animals↗
PubMed1982

Reduced prolactin binding to liver membranes during pheromonal emission in the rat.

Between 14 and 27 days of lactation, female rats excrete a pheromone in their feces that is cholic-acid dependent and that strongly attracts young. Previous research has shown that high circulating levels of prolactin are necessary before the pheromone can be emitted. However, during the time of pheromonal emission prolactin in serum conspicuously declines, while in hepatic cytosol the hormone reaches peak levels. We were interested in the question of how the liver can show peak cytosolic concentrations of prolactin at a time of falling blood levels of prolactin. Accordingly, we examined the prolactin binding capacity of liver membrane fractions during selected periods of lactation. We also studied the livers of virgin and pregnant females for comparison. Three membrane fractions were separated: the cell membrane, the nuclear membrane and a fraction consisting of the cell membrane and large non-nuclear organelles. In all three fractions, there was an increase in available and total prolactin binding in the liver when pregnant females were compared with nulliparous females. However, during the time of pheromonal emission, when prolactin in hepatic cytosol was elevated, there was a significant reduction in the prolactin binding capacity of the liver. How such a reduction increases the cytosolic concentration of the hormone and in turn heightens cholic acid output and pheromonal emission remains unsolved.

Animals↗
PubMed1985

Prolactin-induced polyamine biosynthesis in spleen and thymus: specific inhibition by cyclosporine.

The induction of ornithine decarboxylase (ODC) in the rat spleen and thymus in response to prolactin shows a dose-dependent sensitivity to cyclosporine (CsA), a known immunosuppressive drug. Marked inhibition of prolactin-stimulated ODC activity occurred at 0.12 mg CsA/kg body weight, and nearly total inhibition was detected at 1.2 mg CsA/kg, a dose comparable to that used to suppress organ rejection processes. CsA blocked ODC induction in response to prolactin injection in both intact and hypophysectomized rats, suggestive of a direct effect of prolactin on spleen and thymus. Furthermore, we were able to demonstrate specific 125I-prolactin binding sites on the rat spleen and thymus. Although growth hormone was capable of elevating ODC activity in spleen, this elevation was not inhibited by CsA. ODC activity in response to cyclic AMP-mediated hormones and to steroid analogs such as dexamethasone was not affected by CsA. Agents known to alter calcium channeling mostly had random enhancing capacity when administered with CsA. The most potent elevation occurred in spleens in response to aminophylline plus CsA. It should be noted, however, that aminophylline alone slightly inhibited the basal level of ODC in the spleen. Insulin, which elevated ODC in the thymus and spleen in a dose-dependent manner, also was not affected by concurrent CsA administration. Prolactin administration altered the RNA and DNA content of spleen and thymus indicating its ability to alter metabolic function. We conclude that prolactin may regulate immune function in spleen and thymus. Studies are in progress to identify the regulation of specific gene products by prolactin.

Animals↗
PubMed1986

The ontogeny of specific prolactin binding sites in the rat choroid plexus.

The development of prolactin receptors in the choroid plexus of the rat was examined using the in vivo autoradiographic approach employing the principle of competitive binding. Experimental animals were injected with [125I]prolactin alone (total binding) while control animals received [125I]prolactin and a 500-fold excess of unlabelled prolactin (non-specific binding). Newborns as well as animals 10, 14 and 18 days postnatal were studied. Three minutes following hormone injection animals received an intracardiac perfusion with fixative and tissues were prepared for quantitative light microscopic autoradiography. The choroid plexus first demonstrated specific binding of prolactin, i.e. a statistically significant difference in the autoradiographic reactions between experimental and control animals, at 14 days postnatal. The lactogen specificity of these binding sites was further defined by the ability of [125I]prolactin to be displaced by unlabelled human growth hormone, which is lactogenic in rats, and not by unlabelled insulin, which is structurally dissimilar to prolactin. Morphometric analyses were performed on electron micrographs of choroid plexus from 10- and 14-day postnatal rats. The volume densities of constituents known to be enriched in polypeptide hormone receptors were measured and compared. Small cytoplasmic vesicles and tubules were statistically significantly more abundant in 10-day-old rats than in 14-day-old animals. It is conjectured that these vesicles and tubules contain an intracellular pool of prolactin receptors whose decrease at 14 days parallels the expression of specific binding sites at the cell surface.

Adrenal Cortex↗