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At least 1,153 records · Page 64Linked to original sources
PubMed2002

Elevation of prolactin levels by atypical antipsychotics.

OBJECTIVE: Atypical antipsychotics are thought not to elevate prolactin levels. The authors examined data suggesting that atypical antipsychotics do elevate prolactin levels but more transiently than typical antipsychotics. METHOD: Prolactin levels in 18 male patients with schizophrenia who were receiving atypical antipsychotics were monitored over the 24-hour period following administration of their daily oral dose of risperidone, olanzapine, or clozapine. RESULTS: The baseline prolactin levels in patients receiving risperidone (mean=27 ng/ml, SD=14) were abnormally high, but baseline prolactin levels in patients receiving olanzapine (mean=9 ng/ml, SD=5) and clozapine (mean=9 ng/ml, SD=5) were not high. All three atypical antipsychotics caused a doubling of prolactin levels over baseline levels 6 hours after medication administration. CONCLUSIONS: These data suggest that these atypical antipsychotics raise prolactin levels, although the increases with olanzapine did not reach statistical significance. This suggests that the differences in the effects on prolactin levels of atypical and typical antipsychotics are not categorical but lie in the degree and duration of dose-induced prolactin elevation, attributable to the differential binding properties of each drug on pituitary dopamine D(2) receptors.

Adult↗
PubMedDate not supplied

Thyroid function and release of thyroid-stimulating hormone and prolactin from the pituitary in human obesity.

Thyroid function, basal serum thyroid-stimulating hormone (TSH) and prolactin concentrations, and the effects of 200 micrograms TSH-releasing hormone (TRH) given intravenously on TSH (delta TSH) and prolactin (delta prolactin) were investigated in 25 euthyroid obese subjects and 20 lean controls. No significant differences in serum thyroid hormone concentrations, glucose metabolism parameters, or basal TSH and prolactin concentrations were detected between groups, but a significant (P less than 0.01) increase in delta TSH and a significant (P less than 0.01) decrease in delta prolactin were observed in obese subjects. No significant differences in basal TSH and prolactin were observed in obese men and women compared with corresponding lean controls, but delta prolactin decreased significantly (P less than 0.01) in obese men and women compared with lean controls and TSH increased significantly (P less than 0.01) in obese men and women. No correlation was found between delta TSH or delta prolactin and body mass index. The study suggests that hyper-responsiveness of TSH and hyporesponsiveness of prolactin to TRH in obese subjects can be related to changes in the central serotoninergic system.

Adult↗
PubMed2001

Antipsychotic drugs and obesity: is prolactin involved?

OBJECTIVES: To correlate the anthropometric indexes (Body Mass Index [BMI] and Waist-Hip ratio [WHR]) with the serum prolactin levels in a heterogeneous population of patients treated with typical antipsychotic (AP) drugs. METHODS: We evaluated BMI, WHR, and fasting serum prolactin of inpatients (n = 105) and outpatients (n = 122) treated with APs, in outpatients receiving other psychotropic drugs (OPDs) (n = 77), and in drug-free subjects (n = 33). Outpatients had free access to food, whereas the inpatient sample comprised people with a monotonous diet of approximately 2000 Kcal daily. RESULTS: Prolactin correlated positively with the BMI in the whole group of AP-treated outpatient men (P = 0.03) and with the WHR in AP-treated inpatient men (P = 0.053). Regarding treatment duration, prolactin and BMI correlated positively in men consecutively treated for more than 1 year (P = 0.023). By contrast, a trend toward a negative correlation between prolactin and BMI was observed in AP-treated outpatient women (P = 0.08). No significant correlation, or even a trend, was observed in the other groups. CONCLUSIONS: Prolactin may be involved in AP-induced weight gain, particularly in men. Future studies should characterize the period of maximal prolactin impact on body weight during AP treatment. Specific populations particularly sensitive to hyperprolactinemia might be identified as well. The negative correlation between prolactin and BMI detected in AP-treated women resembles the dampened prolactin response observed in severe primary obesity.

Adult↗
PubMed2005

Integrin activates receptor-like protein tyrosine phosphatase alpha, Src, and Rho to increase prolactin gene expression through a final phosphatidylinositol 3-kinase/cytoskeletal pathway that is additive with insulin.

We previously showed that receptor-like protein tyrosine phosphatase (RPTP)-alpha inhibited insulin-increased prolactin gene transcription. Others suggested that RPTPalpha was a key intermediary between integrins and activation of Src. We present evidence that inhibition of insulin-increased prolactin gene transcription was secondary to RPTPalpha activation of Src, reflecting its role as mediator of integrin responses. Src kinase activity was increased in GH4 cells transiently or stably expressing RPTPalpha and cells plated on the integrin-alpha5beta1 ligand fibronectin. C-terminal Src kinase inactivated Src and blocked RPTPalpha inhibition of insulin-increased prolactin gene transcription. Expression of dominant-negative Src also prevented the RPTPalpha-mediated inhibition of insulin-increased prolactin gene expression. Low levels of a constitutively active Src mutant (SrcY/F) stimulated whereas higher expression levels of Src Y/F inhibited prolactin gene expression. Src-increased prolactin gene transcription was inhibited by expression of a blocking Rho-mutant (RhoN19), suggesting that Src acted through or required active Rho. Experiments with an activated Rho-mutant (RhoL63) demonstrated a biphasic activation/repression of prolactin gene transcription that was similar to the effect of Src. The effects of both Src and Rho were phosphatidylinositol 3-kinase dependent. Expression of SrcY/F or RhoL63 altered the actin cytoskeleton and morphology of GH4 cells. Taken together, these data suggest a physiological pathway from the cell matrix to increased prolactin gene transcription mediated by RPTPalpha/Src/Rho/phosphatidylinositol 3-kinase and cytoskeletal change that is additive with effects of insulin. Over activation of this pathway, however, caused extreme alteration of the cytoskeleton that blocked activation of the prolactin gene.

Animals↗
PubMed2006

Suppression of prolactin-induced signal transducer and activator of transcription 5b signaling and induction of suppressors of cytokine signaling messenger ribonucleic acid in the hypothalamic arcuate nucleus of the rat during late pregnancy and lactation.

During late pregnancy and lactation, the tuberoinfundibular dopamine (TIDA) neurons that regulate prolactin secretion by negative feedback become less able to produce dopamine in response to prolactin, leading to hyperprolactinemia. Because prolactin-induced activation of dopamine synthesis in these neurons requires the Janus kinase/signal transducer and activator of transcription 5b (STAT5b) signaling pathway, we investigated whether prolactin-induced STAT5b signaling is reduced during lactation and whether induction of suppressors of cytokine signaling (SOCS) mRNAs occur at this time and in late pregnancy. During lactation, the ability of exogenous prolactin to induce STAT5 phosphorylation and STAT5b nuclear translocation was markedly reduced when compared with diestrous rats. In nonpregnant female rats, acute treatment with ovine prolactin markedly increased levels of SOCS-1 and -3 and cytokine-inducible SH2-containing protein mRNA in arcuate nucleus micropunches. On gestation d 22, SOCS-1 and SOCS-3 mRNA levels were 10-fold that on G20. SOCS-1 and -3 and cytokine-inducible SH2-containing protein mRNA levels were also elevated on lactation d 7. At these times, dopaminergic activity was decreased and the rats were hyperprolactinemic. The high levels of SOCS mRNA were prevented by bromocriptine pretreatment (gestation d 22) or pup removal (lactation d 7), which suppressed circulating prolactin to basal levels. These results demonstrate that around the end of pregnancy, prolactin loses the ability to activate STAT5b, associated with an increase in SOCS mRNAs. The loss of this stimulating pathway may underlie the reduced tuberoinfundibular dopamine neuron dopamine output and hyperprolactinemia that characterizes late pregnancy and lactation. The high maternal levels of SOCS mRNAs appear to be dependent on prolactin, presumably acting through an alternative signaling pathway to STAT5b.

Animals↗
PubMed1977

Isolation of gamma-amino butyric acid from pig hypothalami and demonstration of its prolactin release-inhibiting (PIF) activity in vivo and in vitro.

A non-retarded fraction with prolactin-release inhibiting factor (PIF) activity obtained by chromatography of a concentrate of porcine hypothalami on carboxymethyl-cellulose was chromatographically distinct from catecholamines. This fraction was purified further by six steps involving chromatography on Sephadex G-25, countercurrent distribution, free-flow electrophoresis, and chromatography on triethylaminoethyl cellulose. The PIF-active substance was isolated and identified as gamma-amino-butyric acid (GABA) by: 1) amino acid analyses using sodium as well as lithium-based buffers for resolution of biological fluids, 2) thin-layer chromatography of underivatized material as well as phenylthiocarbamyl derivatives, and 3) mass spectroscopy. Natural and synthetic GABA inhibited prolactin, but not LH release in vitro from isolated rat pituitary halves at doses as low as 0.1 microgram/ml. The inhibition was proportional to the dose; natural and synthetic GABA possessed identical PIF activity. Synthetic GABA also decreased prolactin release in monolayer cultures of rat pituitary cells and inhibited TRH-stimulated prolactin release. The inhibition of prolactin release in vitro by GABA could not be blocked by perphenazine, which inhibits PIF activity of catecholamines. GABA also suppressed prolactin release in vivo, although large doses were needed. Either rapid iv injection or infusion of GABA in doses of 1 to 100 mg in rats significantly decreased serum prolactin levels, which were previously elevated by pretreatment with monoiodotyrosine perphenazine, chlorpromazine, haloperidol, or sulpiride. beta-hydroxy GABA significantly depressed prolactin release, but beta-(p-chlorophenyl)-GABA (Lioresal, CIBA) and 4 other analogs of GABA were not effective in vivo and/or in vitro. The results indicate that GABA can inhibit prolactin release by a direct action on the pituitary gland, but whether this effect is physiologically meaningful still remains to be determined.

Animals↗
PubMed1975

Surgical disconnection of the medial basal hypothalamus and pituitary function in the rhesus monkey. IV. Prolactin secretion.

The effects of anterior and complete hypothalamic deafferentation on prolactin secretion in the rhesus monkey have been assessed. Complete disconnection ofthe medial basal hypothalamus (MBH) had no apparent effect on serum prolactin concentrations, in either intact or ovariectomized monkeys, nor did it diminish the stimulation of prolactin secretion induced by sodium pentobarbital anesthesia. Anterior disconnection of the MBH in intact females was also without effect on prolactin secretion. When the MBH was inadvertently damaged during the complete disconnection procedure, serum prolactin levels increased approximately 5-fold in otherwise intact animals while remaining unchanged in ovariectomized monkeys, thereby suggesting that ovarian hormones may modulate the secretion of prolactin in response to a reduction of hypothalamic inhibitory influences. In contrast, basal serum prolactin concentrations were not notably influenced by ovariectomy or estrogen administration nor were the patterns of prolactin secretion related to the phases of the menstrual cycle. The results of these studies suggest that the consequences of complete MBH disconnection on prolactin secretion are essentially the same in the rhesus monkey and in the rat, although major differences exist between these species with regard to the influence of estrogen on the production of this hormone.

Animals↗
PubMed1976

Absence of nocturnal elevation of plasma prolactin concentrations in Cushing's disease.

The mean prolactin concentration during sleep and the per cent change (increase) and increment in the nocturnal elevation of plasma prolactin concentrations were significantly reduced (P less than .01, less than .01, and less than .001, respectively) in 6 untreated patients with clinically active Cushing's disease, compared with concentrations seen in normal subjects. There was no significant difference between mean-awake and mean-sleep plasma prolactin concentration in these patients, in contrast to that seen in normal subjects. In contrast, patients with hypercorticism secondary to adrenal adenoma (n = 2) or receiving long-term, high-dose corticosteroid therapy (n = 6) did not differ significantly from normal subjects in the percentage change seen in the nocturnal elevation of their plasma prolactin concentrations. Although mean prolactin concentration during sleep was reduced in these two categories of hypercorticism, a significant difference was still present between mean-awake and mean-sleep plasma prolactin concentration. (The nocturnal increment in plasma prolactin concentrations in these patients with hypercorticism compared with that of normal subjects was reduced, P less than .02). The difference between the percentage change and nocturnal increment observed in patients with Cushing's disease versus that seen in these two categories of hypercorticism was significant at P less than .02 and P less than .01, respectively. Four untreated patients with localized hypothalamic tumors also showed a significant reduction in the percentage change and increment in the nocturnal elevation of plasma prolactin concentrations (P less than .05 and P less than .02). In contrast to these findings, the prolactin responses to thyrotropin-releasing hormone (indicative of pituitary responsiveness) in patients with Cushing's disease, patients with adrenal adenoma, or those receiving chronic corticosteroid therapy, were all within the normal range seen in sex-matched control subjects. These findings provide additional evidence for the suggestion that there is altered hypothalamic function in patients with Cushing's disease.

Adrenal Cortex Hormones↗
PubMed1975

A receptor site for prolactin in lactating mouse mammary tissues.

Prolactin iodinated by lactoperoxidase method showed immunologically, electrophoretically and biolo9gically similar properties to native prolactin and possessed enough specific radioactivity for receptor studies. 1251-prolactin was incubated with mouse mammary tissues at 8 days of lactation. Both binding and release of 1251-prolactin depended on incubation time and temperature and were maximal at 37 degrees C. Michaelis constant was estimated to be 1.4 X 10(-9) M from Lineweaver-Burk plot and to be 1.2 X 10(-9) M from id-value of the dose-response curve for displacement with native prolactin. Total number of binding sites for prolactin was 1.38 X 10(-15) mole per mg weight of tissue. Ovine prolactin, human growth hormone and human placental lactogen complete with 1251-prolactin and dose-response curves for these three hormones were all parallel. These results suggest the existence of a specific receptor site with high affinity for prolactin in lactating mouse mammary glands.

Animals↗
PubMed1978

Cord serum prolactin in relation to the time of the day, the sex of the neonate and the birth weight.

Serum prolactin was measured in 581 blood samples collected immediately after birth from 563 single new-born and from 9 pairs of twins. Cord serum prolactin is high at birth: the mean level is some 5 times higher than in adults. There is no sex difference in cord serum prolactin concentration in the neonate. Mean serum prolactin is significantly higher at 1.00 and 2.00 a.m. Thus a circadian periodicity in serum prolactin concentration seems to appear already during foetal life well before the organization of sleep rhythm. Cord serum prolactin increases with birth weight ranging from 1500 g to 3500 g. Thus, the control of levels of circulating prolactin changes during foetal life resulting in a progressive increase starting from mid-pregnancy. Mean cord serum prolactin at birth is lower in twins than in single new-borns. There is no significant difference in serum prolactin between the first and the second twin.

Birth Weight↗
PubMed1979

Persisting suppression of prolactin secretion after long-term treatment with bromocriptine in patients with prolactinomas.

The effect of bromocriptine withdrawal after long-term treatment on prolactin levels has been investigated in thirty-seven patients with prolactinomas. In ten patients with macroprolactinomas and post-operatively excessively high prolactin levels persisting suppression of prolactin secretion after bromocriptine withdrawal has been observed. This effect was not observed in patients with microprolactinomas or macroprolactinomas with only moderately elevated prolactin levels. The degree of persisting suppression correlated to the height of prolactin levels before treatment and to the duration of bromocriptine therapy. No correlation was found between the rise of prolactin levels after bromocriptine withdrawal and withdrawal time. It is suggested that the persisting suppression of prolactin levels is a sequence of reduction in tumour size. This anti-proliferative action of bromocriptine seems to be specific for the prolactin secreting cells in macroprolactinomas with high proliferation rate and high prolactin turn-over. These findings offer new possibilities in the management of patients with macroprolactinomas.

Adenoma↗
PubMed1984

Prolactin in hirsute women: possible roles for androgens in suppressing basal levels, and for oestrogens in enhancing TRH-induced responses.

Hyperprolactinaemic patients occasionally demonstrate hirsutism and elevated levels of DHA-S, a weak androgen of adrenal origin. Abnormal adrenal function is frequently observed in hirsute patients. These observations prompted speculation that prolactin may modulate normal adrenal secretion and that derangements of adrenal androgen secretion may be due to abnormalities in prolactin. In this study we examined the possibility that elevated prolactin levels may be involved in the pathogenesis of hyperandrogenaemia in hirsute patients. However, basal prolactin levels in hirsute women, with or without menstrual disturbances, 201 +/- 24.3 mU/l (mean +/- SE) and 192 +/- 24.3 mU/l respectively, were significantly suppressed below levels in normal women, 289 +/- 12.2 mU/l. The prolactin responses to stimulation with TRH and to suppression with L-dopa were also studied in hirsute patients. The prolactin response to TRH (maximum increment or integrated response) was exaggerated significantly in hirsute women with menstrual disturbances when compared to normal women, to hirsute women with normal menses or to normal men. This abnormal response may have been due to elevated oestrone levels present in patients with oligomenorrhoea (318 +/- 49.5 pmol/l compared to 191 +/- 12.1 pmol/l in normal women and 161 +/- 15.5 pmol/l in hirsute women with normal menses, P less than 0.05). There were no abnormalities detected in the suppression of prolactin in response to L-dopa in any of these groups. These findings do not support a role for prolactin in the pathogenesis of hyperandrogenaemia in hirsute patients. However, elevated androgen levels in women may bring about suppression of basal prolactin levels to values seen in normal men. (ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1989

Development of progesterone dependency in the appearance of the nocturnal prolactin surge in immature rats.

Basal concentrations of plasma prolactin in immature, Wistar-Imamichi strain rats at 25, 28 and 31 days of age were 5-12 ng/ml and no prolactin surges were observed in intact immature rats. Plasma progesterone values ranged from 5 to 9 ng/ml, while plasma oestradiol concentrations increased from 11 to 27 pg/ml between 25 and 31 days of age. When oestradiol was administered to ovariectomized 25- or 28-day-old rats by s.c. insertion of an implant, plasma prolactin concentrations at 05:00 and 12:00 h were similarly elevated 3 days after the operation. Oestradiol did not induce a nocturnal prolactin surge. The progesterone implants in ovariectomized rats at 28 days of age or on the first day of oestrus increased plasma prolactin values at 05:00 h. The magnitude of the progesterone-induced prolactin surge was greater when progesterone was given closer to the time of the first ovulation (about 34 days old). Pretreatment with oestradiol amplified the progesterone-induced prolactin surge. Mechanisms causing nocturnal prolactin surges are more sensitive to, and respond over a longer time period, to progesterone in pubertal rats than in adult animals. The results suggest that progesterone initiates the nocturnal surge of prolactin release and that oestradiol can amplify the effects of progesterone.

Animals↗
PubMed1989

Effects of prolactin on conceptus survival and uterine secretory activity in pigs.

Hypoprolactinaemia was induced by bromocriptine (CB154; 100 mg/day) which decreased circulating prolactin by 40% (P less than 0.06), but did not affect conceptus survival at Day 25 when administered on Days 10-16 when compared to saline:ethanol-treated control gilts. Bromocriptine or vehicle was administered to cyclic gilts on Days 10-11, oestradiol valerate was injected on Day 11 and uterine flushings were collected on Day 12. Total recoverable protein and uteroferrin in uterine flushings were not affected by treatment. However, leucine aminopeptidase activity (P less than 0.02) and total recoverable Ca2+, Na+, K+ and Cl- (P less than 0.05) were decreased in uterine flushings of gilts that received bromocriptine, suggesting that hypoprolactinaemia decreased general secretory activity of the endometrial epithelium and modulated ionic changes, respectively, in the uterine environment of pigs. Subcutaneous administration of pig prolactin (1 mg/12 h) increased (P less than 0.001) serum prolactin 4.5-fold. The interaction between hyperprolactinaemia and progesterone, without oestrogen, on components of uterine flushings were determined using gilts that received progesterone (200 mg/day) and prolactin or saline on Days 4-14 after ovariectomy on Day 4. On Day 15, there were no differences (P greater than 0.05) in any of the uterine secretory components measured. Hyperprolactinaemia (1 mg pig prolactin on Days 6-11) enhanced overall uterine secretory response on Day 12 to oestradiol (5 mg) administered on Day 11 compared to gilts that received 1 ml saline on Days 6-11 of the oestrous cycle. Total recoverable protein and leucine aminopeptidase activity were greater (P less than 0.05) for oestradiol-treated gilts, but effects of prolactin were not significant. Total recoverable glucose (P less than 0.01), PGF-2 alpha (P less than 0.02), uteroferrin (P less than 0.01) and specific activity of uteroferrin (P less than 0.001) were increased by prolactin and oestradiol, but not oestradiol alone. Calcium (P less than 0.05), chloride (P less than 0.05) and potassium (P less than 0.01) were increased in response to oestradiol. These results indicate an interaction between oestradiol and prolactin, but not progesterone and prolactin, which enhances secretion of some products of the pig uterine endometrium.

Animals↗
PubMed1990

Correlation with changes in horns and pelage, but not reproduction, of seasonal cycles in the secretion of prolactin in rams of wild, feral and domesticated breeds of sheep.

Seasonal cycles were monitored in groups of wild (mouflon), feral (Soay) and domesticated breeds of sheep (Shetland, Blackface, Herdwick, Norfolk, Wiltshire, Portland, Merino, Soay x Portland and Soay x Merino) living outdoors near Edinburgh (56 degrees N). Changes in the blood plasma concentrations of prolactin and FSH, and growth of the horns and pelage were measured every half calendar month from 1 to 3 years of age. In all breeds there was a clearly defined seasonal cycle in the plasma concentration of prolactin with an 18-66-fold increase in mean values from the nadir in November and December to the peak in May and June. The seasonal increase in prolactin was closely correlated with the seasonal increase in the growth of the horns, both within and between breeds (e.g. time of peak prolactin vs horn growth for 11 breeds, R = 0.62, P less than 0.05). In the mouflon, Soay and some of the domesticated breeds of sheep (Wiltshire, Herdwick and Shetland), the seasonal increase in prolactin was also temporally correlated with the resurgence of growth of the pelage in spring and a conspicuous moult. In the other breeds developed to produce fine wool (e.g. Norfolk, Portland and Merino), there was no clear seasonal change in the pelage and growth continued throughout the year. Comparison between breeds indicated that continuous growth of the pelage was associated with higher plasma prolactin concentrations in winter. The times of the seasonal changes in plasma concentrations of prolactin were not significantly correlated with the corresponding changes in the plasma concentrations of FSH. The overall results are consistent with a role for prolactin related to the growth of the horns and pelage rather than the seasonal cycle in reproduction. The differences between the wild-type and the domesticated breeds in the pelage represent the effect of selective breeding to produce a long fine fleece which has involved changes in both the seasonal pattern of prolactin secretion and the growth characteristics of the hair fibres.

Animals↗
PubMed1993

Differential effects of adrenalectomy on the prolactin-induced suppression of LH and FSH secretion after castration in male rats.

Hyperprolactinaemia inhibits gonadotrophin secretion in males and females of many species. The aim of this study was to determine the role of the adrenal gland in mediating the inhibitory effects of prolactin by contrasting the effects of acute hyperprolactinaemia on LH and FSH secretion in adrenal-intact and adrenalectomized rats with and without physiological corticosterone replacement. Adult male rats were administered purified ovine prolactin every 12 h (2.4 mg per injection s.c.) beginning at the time of castration. Blood samples were collected every 3 h for 36 h, then every 12 h until 10 days after castration. Ovine prolactin significantly reduced LH secretion in all groups from approximately 15 to 48 h after castration. In contrast, plasma FSH concentrations were reduced by ovine prolactin from 21 to 48 h only in the adrenal-intact rats and not in the adrenalectomized or adrenalectomized plus corticosterone groups. In all groups, ovine prolactin inhibited endogenous prolactin secretion in rats by short-loop autofeedback as soon as 3 h after the first ovine prolactin injection and throughout the 10 days of the study. Adrenalectomy per se, with or without corticosterone replacement, also had a differential effect on LH and FSH secretion after castration, causing only a transient delay in the rise in LH after castration, but inducing a significant and long-lasting inhibition of FSH secretion. The results demonstrate that ovine prolactin-induced suppression of LH secretion after castration occurs with or without the adrenal glands. Suppression of FSH secretion after castration by ovine prolactin, however, may involve an adrenal component.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1988

Calcium dependence of prolactin mRNA accumulation in GH3 rat pituitary tumour cells.

Stimulation of prolactin secretion by TRH probably involves mobilization of intracellular calcium to a greater extent than calcium influx, but less is known about the possible calcium-dependent mechanisms which may control prolactin gene transcription. We have studied this question in the rat pituitary tumour GH3 cell line by measuring prolactin mRNA accumulation by a cytoplasmic dot hybridization assay. Cobalt chloride, an intracellularly acting calcium antagonist, caused marked dose-dependent reductions in prolactin release and mRNA concentrations, whereas the calcium channel-blocking agent verapamil had no effect on prolactin release and had smaller effects on prolactin mRNA. Cobalt chloride abolished the stimulatory effect of TRH on prolactin mRNA levels, while verapamil caused only moderate inhibition. Growth hormone mRNA levels in the same cells were not significantly affected by TRH or verapamil, and only marginally reduced by cobalt. These data suggest that, as for prolactin release from normal rat pituitary lactotrophs, prolactin mRNA accumulation in GH3 cells appears to have a requirement for intracellular calcium which is only partly dependent upon calcium influx.

Calcium↗
PubMed1980

Roles of prolactin, growth hormone, insulin and thyroxine in steroid-induced lactation in goats.

Plasma concentrations of prolactin, growth hormone, insulin and thyroxine have been examined in relation to mammary growth and lactation induced by oestradiol benzoate (OB) and progesterone in ten virgin female goats. A daily injection of OB (250 microgram) and progesterone (60 mg) stimulated a significant, accumulative increase in prolactin in the circulation after 15 and 65 days and this was accompanied by udder growth. No increase in udder size was observed when prolactin was maintained at basal concentrations by simultaneous daily injections of the prolactin-inhibitor, bromocriptine (5 mg). Increasing the daily dose of OB (2.5 mg) and decreasing that of progesterone (6.25 mg) led to a further increase in both plasma prolactin and udder size and stimulated the onset of copious lactation. When prolactin was maintained close to basal concentrations throughout the periods of steroid treatment milk secretion was almost totally inhibited. There was some evidence that steroid treatment enhanced the prolactin response to milking and that additional quantities of bromocriptine were necessary to inhibit the secretion of prolactin when the pituitary gland was exposed to steroid stimulation. There were no marked changes in growth hormone, insulin or thyroxine in the circulation until the start of milking. It is concluded that the presence of increased quantities of prolactin in the blood are essential for the successful induction of mammary growth and lactation with OB and progesterone in virgin goats.

Animals↗