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PubMed2000

Gonadotroph-lactotroph associations and expression of prolactin receptors in the equine pituitary gland throughout the seasonal reproductive cycle.

An interaction between gonadotroph and lactotroph cells of the pituitary gland has long been recognized in several species. The current study was conducted to investigate whether an association between gonadotrophs and lactotrophs occurs in mares and whether prolactin receptors are expressed within the pituitary gland of this species. The effects of both reproductive state and season on these variables were examined in pituitary glands obtained from sexually active mares in July (breeding season), sexually active mares in November (non-breeding season) and anoestrous mares in November. Pituitaries were dissected out immediately after death and immunofluorescent staining was carried out on 6 micrometer sections using specific antibodies to the LHbeta subunit, FSHbeta subunit, prolactin and prolactin receptor. Gonadotrophs were observed in both the pars distalis and pars tuberalis; although they appeared mostly as isolated cells, small groups of gonadotrophs were also identified in the pars distalis. In contrast, lactotrophs were observed only as clusters of cells exclusively in the pars distalis of sexually active and anoestrous mares in November and in most of the sexually active mares in July. A specific gonadotroph-lactotroph association was identified only between large isolated gonadotrophs and lactotroph clusters. Double immunofluorescent staining for FSHbeta and prolactin revealed a similar gonadotroph-lactotroph association to the one detected for LH gonadotrophs. No statistical difference in the gonadotroph:lactotroph ratio was observed as a result of changes in reproductive status or season. However, a tendency for a simultaneous decrease in the number of gonadotrophs and an increase in the number of lactotrophs was detected in anoestrous animals. Prolactin receptor immunoreactivity was found in the pars distalis, but not in the pars tuberalis, of sexually active (July and November) and anoestrous animals for both long and short forms of the receptor. No prolactin receptor co-localization for either form of the receptor was observed in LH or FSH gonadotrophs in either of the reproductive states examined during both summer and winter seasons. Furthermore, no significant difference was apparent in the proportion of cells expressing prolactin receptors between mares of different reproductive state or season. The specific anatomical association between gonadotroph and lactotroph cells and the expression of prolactin receptors in the equine pituitary gland indicate a potential role of prolactin in the regulation of gonadotrophin secretion. However, the absence of evidence for co-localization of prolactin receptors in LH or FSH cells does not support the hypothesis of a direct effect of prolactin on the gonadotroph as reported in a short day breeder. The results raise the possibility that, in horses, an intermediate regulatory cell may mediate the action of prolactin on gonadotroph function.

Animals↗
PubMed1976

Prolactin binding to mammary gland, 7,12-dimethylbenz(a)-anthracene-induced mammary tumors, and liver in rats.

Specific binding of radioactively labeled prolactin was determined in membrane preparations from mammary glands and livers of rats during pregnancy and lactation. Prolactin binding to mammary gland increased throughout late pregnancy and early lactation, reached a maximum on Day 11 of lactation, and then declined. Maximum prolactin binding to liver membrane preparations was observed during late pregnancy and declined throughout lactation. Estradiol benzoate (20 mug/day), administered on Days 5 to 10 of lactation, reduced prolactin binding to mammary gland by 55%, increased binding to liver 2-fold, and reduced litter weight gain by 25%. Prolactin binding to 7,12-dimethylbenz(a)anthracene-induced mammary tumors was 3 times higher than that observed in lactating mammary gland. Administration of prolactin enhanced tumor growth but decreased specific prolactin binding to tumors. Lergotrile mesylate inhibited and estradiol benzoate (2 mug/day) enhanced tumor growth, but neither treatment affected prolactin binding to tumor membrane preparations. In contrast, higher doses of estradiol benzoate (20 mug/day) inhibited tumor growth and reduced prolactin binding. Prolactin binding varied widely within all groups of mammary tumors and was not clearly related to growth response or to altered circulating estrogen and/or prolactin levels. Hormone dependence in this animal tumor model is complex and may not be predicted on the basis of prolactin-binding capacity alone.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1989

Prolactin is transported across the epithelium of the jejunum and ileum of the suckling rat.

Milk prolactin is transferred from the gastrointestinal tract to the circulation of the suckling rat. To identify the site of prolactin penetration and to determine the mechanism by which the hormone traverses the mucosal barrier, we followed the uptake of prolactin from ligated loops of jejunum or ileum in vivo by three methods: autoradiography, transport of prolactin-gold conjugates, and immunocytochemistry. Autoradiographic studies demonstrated specific binding sites for 125I-prolactin on apical membranes of the jejunum and ileum. Excess cold prolactin reduced radiolabel in apical and basal compartments. Gel autoradiography of portal sera showed the presence of intact prolactin and a prolactin fragment following jejunal transport but only a prolactin fragment following ileal transport. Uptake of prolactin-gold conjugates demonstrated that, in the jejunum, label was present at the luminal surface, within endosomal compartments and lysosomes, in basal coated and smooth vesicles, within basal coated pits, and beyond the basolateral surface. In the ileum, label was found at the luminal surface; within the tubulocisternae, endosomal vesicles, lysosomes, and basal smooth vesicles; and beyond the basolateral surface. Immunoreactive prolactin was present throughout the transepithelial pathways. This study demonstrates that prolactin is selectively and nonselectively absorbed in the jejunum and ileum and that the hormone is directed either to the lysosome for degradation or across the epithelium by means of a transcellular pathway.

Animals↗
PubMed1995

Prolactin specifically increases pyruvate dehydrogenase E1 alpha in rat lateral prostate epithelial cells.

Prolactin is an important regulator of prostate citrate production. In rats this regulatory effect of prolactin is specific for lateral prostate, and has no effect on either ventral or dorsal prostate. The mechanisms by which prolactin regulates prostate citrate production have not been elucidated. Two key regulatory enzymes involved in citrate synthesis by prostate epithelial cells are mitochondrial aspartate aminotransferase (mAAT) which provides oxalacetate, and PDH E1 alpha (pyruvate dehydrogenase) which provides acetyl CoA for citrate synthesis. Our previous studies demonstrated that prolactin regulates mAAT. However, an increase in citrate synthesis would require an increase in both oxalacetate and acetyl CoA. Therefore, we investigated the possibility that prolactin might also regulate PDH E1 alpha in LP epithelial cells. The present studies demonstrate that prolactin administration (1 mg/rat) to rats resulted in an increased level of E1 alpha in LP epithelial cells within 6 hr, but had no effect on the E1 alpha level of VP epithelial cells. In vitro studies demonstrated that exposure of freshly prepared LP epithelial cells to prolactin (0.1-1.0 microgram/ml) resulted in increased levels of E1 alpha. Prolactin had no effect on either VP or DP epithelial cells. The stimulatory effect of prolactin on E1 alpha was inhibited by actinomycin and cycloheximide, thereby indicating that prolactin stimulated the biosynthesis of E1 alpha. The studies reveal that prolactin specifically stimulates E1 alpha levels of LP epithelial cells, whereas testosterone specifically stimulates E1 alpha levels of VP epithelial cells. At this time, we propose that the effects of prolactin and testosterone involve increased expression of the E1 alpha gene of LP and VP epithelial cells, respectively.

Animals↗
PubMed1996

Parental care and the prolactin secretion pattern in the King penguin: an endogenously timed mechanism?

The King penguin (Aptenodytes patagonicus) has been studied on Possession Island, Crozet Archipelago (46 degrees 25'S-51 degrees 45'E). It is an offshore feeder, but it breeds on land. Its breeding cycle is unusually long (about 14 months). It starts at the beginning of spring, is interrupted during 5 months of winter, and ends in the next spring. Furthermore, it is characterized by a long parental care period, of about 11 months, including the winter interruption. In fact, care given to the egg and the chick is biparental, which supposes that parental behavior includes both parents. Each parent alternates care given to the egg and to the chick on land and foraging bouts at sea. An incubation bout, or a chick care bout, is called a shift. Prolactin is the hypophyseal hormone known to be correlated with incubation and chick care. We studied the mechanism of the maintenance of prolactin during the parental care period in the King penguin, a period which is unusually long. In many species, prolactin secretion has been shown to be stimulated by the presence of eggs and/or chicks, but in the King penguin, prolactin secretion is observed throughout the entire period of parental care, despite the fact that the birds leave the egg and the chick repeatedly and for extended periods of time to feed. Prolactin levels rise significantly at the beginning of courtship; females have significantly higher prolactin levels than males during courtship, copulation, and the period of waiting for egg laying. In both sexes, prolactin levels remain high during incubation and the first part of chick rearing, before winter. Prolactin concentrations decline somewhat during the winter period of minimal parental care, but remain that level in spring when parental care starts again. The level returns to basal value during molt. Prolactin levels rise during the incubation shifts but not over the course of contact with young. Prolactin values remain high in unsuccessful breeders, possibly preventing the birds from relaying, but remain low in immature birds. These data raise questions about how prolactin secretion is controlled in this species. The hypothesis of a programmed secretion of prolactin is advanced.

Animals↗
PubMed1994

Immunoendocrine mechanisms in mammary tumor progression: direct prolactin modulation of peripheral and preneoplastic hyperplastic-alveolar-nodule- infiltrating lymphocytes.

We have previously shown that the immunoregulatory function of prolactin may play a role in the progression of the mouse mammary preneoplastic hyperplastic alveolar nodule (HAN) line C4 to carcinoma. In this study we investigated the direct effect of prolactin on lymphocytes isolated from normal and C4-HAN-bearing mice. In addition, we tested the effect of ovariectomy on prolactin/lymphocyte interaction to see whether, as has been reported in rats [Mukherjee P., Hymer W. C. (1992) Prog Neuroendocrinol Immunol 5: 108; Viselli S. M. et al. (1991) Endocrinology 129: 983], removal of estrogen would enhance the response to prolactin in mice. Proliferation of splenocytes, lymph node cells and HAN-infiltrating lymphocytes was stimulated by prolactin in a dose-responsive fashion. Ovariectomy did not alter this effect consistently. Cell-cycle analysis based on simultaneous staining of DNA and RNA revealed that prolactin-stimulated lymphocytes progress through all phases of the cell cycle whereas anti-prolactin antiserum inhibits this stimulation. Two-color flow-cytometric analysis revealed the time-dependent induction of interleukin-2 (IL-2) receptor expression on both CD4+ and CD8+ cells by prolactin. Prolactin-treated lymphocytes also produced low yet detectable levels of bioactive IL-2 in a dose- and time-dependent fashion. Prolactin enhanced lymphocyte responsiveness to mitogens and showed a marked synergism at suboptimal concentrations. Pretreatment of splenocytes from HAN bearers with a high concentration of prolactin slightly enhanced natural killer (NK) activity; anti-prolactin antiserum reduced the NK lytic activity of poly(I).poly(C)-activated splenocytes from HAN-bearing mice. Our results provide direct experimental evidence for the stimulatory effect of prolactin on lymphocyte function and IL-2-mediated lymphocyte proliferation and suggest a mechanism linking the endocrine system to immunomediated enhancement of HAN progression.

Animals↗
PubMed1998

The effect of acute or chronic administration of prolactin on renal function in feral chickens.

The role of the hormone prolactin in avian osmoregulation has not been clearly defined. The increases in plasma prolactin concentrations which have been demonstrated in previous studies in response to osmotic stress are strongly suggestive of a role for prolactin in avian osmoregulation. The present study investigated the effects of either acute or chronic administration of ovine prolactin on plasma electrolytes and renal function in the feral chicken. The effect of acute administration of prolactin depended on the dose of prolactin used. All plasma concentrations of prolactin achieved by the infusions were greater than reported values for endogenous prolactin. Acute infusion of prolactin at the lower dose increased the fractional excretion of sodium and chloride significantly, whereas the higher dose of prolactin had no effect. However, chronic administration of ovine prolactin had no significant effects on plasma electrolytes and renal function. It is possible that the role of prolactin in avian osmoregulation is a combination of its effects on the kidneys and also on extrarenal tissues such as the intestine and nasal salt glands (where present).

Animals↗
PubMed1986

Inhibition of human chorionic gonadotropin production by prolactin from term human trophoblast.

In vivo suppression of prolactin concentrations by bromocriptine near term, in a pregnant woman with a prolactinoma, was followed by augmentation of human chorionic gonadotropin levels. Suspension of drug therapy at 38 weeks of gestation was followed by a reversal of this sequence of events. In vitro, both ovine prolactin and human prolactin added to explants of term placental trophoblast significantly inhibited human chorionic gonadotropin production from this tissue. Although, with ovine prolactin, this inhibitory effect was demonstrable up to 5 micrograms/ml of ovine prolactin in the culture medium, only doses of 0.1 to 0.2 micrograms/ml of human prolactin significantly suppressed human chorionic gonadotropin production. Overall, 0.1 and 0.2 micrograms/ml of ovine prolactin and human prolactin most consistently suppressed human chorionic gonadotropin production to a statistically significant extent. In general, the concentrations in the culture medium of both ovine prolactin and human prolactin that inhibited human chorionic gonadotropin production in vitro were comparable to the concentrations of prolactin present in the mother and fetus. These in vivo and in vitro observations suggest that prolactin inhibits human chorionic gonadotropin production from term human trophoblast.

Adult↗
PubMed1986

The effect of prolactin on fanning behavior in the male three-spined stickleback, Gasterosteus aculeatus L.

The effect of administration of homologous prolactin on fanning behavior, an important aspect of parental care in sticklebacks and many other teleost fish, was studied. Prolactin was administered by implantation of an additional pituitary prolactin lobe in the dorsal body musculature of males with a nest without eggs. The low but rather constant level of fanning behavior is significantly increased from Day 6 to Day 12 after administration of the prolactin lobe. The implantation has no noticeable effects on cell and nuclear size or on the ultrastructure of the in situ prolactin cells of the recipient fish. Recovered prolactin lobe implants show two categories of prolactin cells. The major category consists of cells that are well developed and, similar to in situ prolactin cells, show structural signs of high secretory activity. The other prolactin cell category in the implants shows signs of cellular involution. Ten days after implantation, the first category predominates, and 16 days after implantation the second category. Prolactin lobe implantation increases the number of mucocytes in the epithelium of the skin, in particular at Day 10, and to a lesser extent at Day 16. This is considered evidence for a transient rise in blood prolactin levels in the recipient fish. We conclude that prolactin stimulates fanning behavior in male sticklebacks.

Animals↗
PubMed1991

Comparison of efficacy of cysteamine in depleting prolactin immunoreactivity in different hyperprolactinemic animal models.

We have examined the effects of cysteamine on its ability to deplete prolactin in various states of hyperprolactinemia. Administration of subtoxic doses of cysteamine (75 and 150 mg/kg,sc) dramatically reduces serum prolactin levels as well as pituitary prolactin content in a dose-dependent manner in estrogen-primed brown Irish ACI female rats. A similar dose-dependent decrease in anterior pituitary prolactin levels was observed in two ectopic prolactin secreting pituitary tumor models (MtTW15 and 7315a). However, a significant reduction in serum prolactin levels was seen in these same tumor bearing animals at only the 150 mg/kg dose of cysteamine. Interestingly, the prolactin content of each of the prolactin secreting tumors, although reduced by cysteamine administration, the effect was neither dose-dependent nor as dramatic as that observed in the anterior pituitary gland proper. These data demonstrate that cysteamine can significantly lower prolactin concentrations in hyperprolactinemia. Further, ectopic prolactin secreting pituitary tissue appears less sensitive to the prolactin-depleting effects of cysteamine. This latter finding may explain, in part, why serum prolactin levels were not as severely reduced in the ectopic tumor bearing female rats as in estrogen-induced hyperprolactinemic animals.

Analysis of Variance↗
PubMedDate not supplied

Molecular homology between prolactin and ovarian peptides: evidence for physiologic modification of the parent molecule by the target.

In recent years, prolactin has come to be recognized as an inhibitory gonadotrophin, with the ovarian follicular compartment as its target. In parallel with this, is evidence that granulosa cells give rise to substances secreted into follicular fluid that mimic the inhibitory actions of prolactin, but appear to be oligopeptides. The question that was examined here was whether these peptides are prolactin fragments. The endpoint was immunohistochemical reactivity in ovarian follicles of cycling rats. Antisera to homologous pituitary prolactin were used with and without modification by admixture either of highly purified rat pituitary prolactin or of follicular fluid enriched in prolactin-like bioactivities and depleted of peptides larger than 2000 MW. In growing follicles, immunohistochemical reactions, dependent upon unmodified anti-rat prolactins, occurred in all three follicular compartments but the microdistribution patterns and intensity of the reactions varied within follicles at different stages of development. These differences were compatible with the biological role of prolactin as an inhibitory gonadotrophin. Evidence that the reactions were dependent upon pituitary-like prolactin, present in the follicle, was obtained with highly purified rat prolactin which completely abolished reaction potential of the antisera in all follicles, at all stages. In contrast, the results with antisera to which oligopeptide follicular fluid had been added were end-point dependent; both partial and complete loss of antiserum potency, dependent upon cycle stage and sub-compartmentation of individual follicles were observed. These findings demonstrate molecular homology between pituitary prolactin and what appear to be small peptides of penultimate follicular origin and they lend support to the proposal that the mechanisms of action of prolactin involve modification of the parent molecule by the target.

Animals↗
PubMed2004

Prolactin as a modulator of B cell function: implications for SLE.

Prolactin is not only a lactigenic hormone but also an immunomodulator involved in lymphocyte survival, activation and proliferation. There is increasing data implicating prolactin in autoimmunity, and specifically in SLE. Increased serum prolactin levels have been reported in lupus patients of both genders, and have been associated with accelerated disease expression and early mortality in lupus-prone mice. Furthermore, suppression of prolactin secretion with bromocriptine provides beneficial effects in murine lupus, and perhaps in some SLE patients as well. Treatment with prolactin that causes mild to moderate hyperprolactinemia, similar to that present in SLE patients, breaks tolerance and induces a lupus-like illness in non-spontaneously autoimmune mice with a susceptible genetic background. These immuno stimulatory effects of prolactin are mediated by a decrease in negative selection and the maturation of autoreactive B cells to the follicular subset. Consistent with the fact that follicular B cells are T cell dependent, CD4+ T cells are necessary for the prolactin-mediated break down of B cell tolerance. In mice, the effects of prolactin on the immune system are genetically determined, suggesting that only a subset of SLE patients are likely to have a prolactin-responsive disease. The manipulation of serum prolactin or, even more specifically, follicular B cells that are susceptible to the immuno stimulatory effects of prolactin, may provide novel therapeutic options for those SLE patients with a prolactin-modulated disease.

Animals↗
PubMed2006

Tachykinins and the control of prolactin secretion.

Tachykinins are present in the pituitary gland and in brain areas involved in the control of the secretion of pituitary hormones. Tachykinins have been demonstrated to stimulate prolactin release acting directly on the anterior pituitary gland. These peptides have also been revealed to be able to act at the hypothalamic level, interacting with neurotransmitters and neuropeptides that have the potential to affect prolactin secretion. Tachykinins seem to act by stimulating or inhibiting the release of the factors that affect prolactin secretion. Among them, tachykinins have been demonstrated to stimulate oxytocin and vasopressin release, which in turn results in prolactin release. Tachykinins also potentiated the response to vasoactive intestinal peptide (VIP) and reinforced the action of glutamate, which in turn result in prolactin release. They have also been shown to interact with serotonin, a neurotransmitter involved in the control of prolactin secretion. In addition, tachykinins have been shown to inhibit GABA release, a neurotransmitter with prolactin-release inhibiting effect. This inhibition may result in an increased prolactin secretion by removal of the GABA inhibition. On the other hand, tachykinins have also been shown to stimulate dopamine release by the hypothalamus, an action that results in an inhibition of prolactin release. Dopamine is a well known inhibitor of prolactin secretion. In conclusion, although tachykinins have been shown to have a predominantly stimulatory effect on prolactin secretion, especially at the pituitary level, under some circumstances they may also exert an inhibitory influence on prolactin release, by stimulating dopamine release at the hypothalamic level.

Humans↗
PubMed1996

The effect of prolactin on casein kinase II, MAP kinase and PKC in rabbit mammary cells and Nb2 rat lymphoid cells.

Prolactin induces milk protein gene expression in rabbit primary mammary cells without any concomitant cell multiplication. Prolactin or other lactogenic hormones is the major inducer of cell division in the rat lymphoid Nb2 cells. In Nb2 cells, prolactin also rapidly induces the expression of the c-myc gene, and beta-actin and stathmin gene expression is induced more slowly. The possible involvement of casein kinase II (CKII), mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) in these process is not well known. The present work was undertaken to evaluate the effect of prolactin on these protein kinases and to determine the possible involvement of these enzymes in the activity of several genes under the control of the hormone. In rabbit mammary cells, prolactin did not alter CKII activity but did transiently stimulate MAP kinase activity. Prolactin also stimulated Ca(2+)-independent PKC. This effect was visible after 10 min and was maintained for at least 24 hr. Staurosporine, an inhibitor of PKC and of several tyrosine kinases altered Ca(2+)-independent PKC only moderately. In contrast, GF 109203X, a potent and specific inhibitor of PKC, abrogated almost all PKC activity. Staurosporine, but not GF 109203X, prevented the induction of the casein gene by prolactin. In Nb2 cells, prolactin induced a slow stimulation of CKII activity. The hormone did not induce MAP kinase activity. Prolactin stimulated Ca(2+)-independent PKC over periods of 24 hr. GF 109203X, but not staurosporine, inhibited PKC activity, whereas staurosporine but not GF 109203X, inhibited the induction of Nb2 cell multiplication and the accumulation of c-myc, beta-actin and stathmin mRNAs. From these data, it can be concluded that (1) the stimulation of CKII by prolactin in Nb2 cells is concomitant with cell multiplication: (2) MAPK stimulation is not necessary for prolactin to induce Nb2 cell multiplication; and (3) PKC is stimulated in mammary and Nb2 cells, but this stimulation is not required for prolactin to stimulate casein, c-myc, beta-actin and stathmin gene expression and Nb2 cell division.

Animals↗
PubMed1998

Change in plasma prolactin and clinical response to haloperidol in schizophrenia and schizoaffective disorder.

There has been a long-standing interest in plasma prolactin as a potential in vivo indicator of blockade of tuberoinfundibular D2 dopamine receptors. Potential relationships between prolactin response and neuroleptic treatment have been obscured by the use of high doses which have caused prolactin to plateau. With lower doses of neuroleptic now commonly in use, prolactin may be more valuable as a correlate of clinical response. In this study, 23 acutely exacerbated schizophrenic and schizoaffective patients were washed out for at least 6 days and were then treated with haloperidol to achieve fixed low to moderate plasma levels under double-blind conditions. Clinical response, plasma prolactin, and haloperidol plasma levels were measured weekly for 3 weeks. Clinical symptoms at endpoint were related to both prolactin change and final prolactin level during haloperidol treatment. Specifically, fewer symptoms at endpoint were associated with a greater increase in prolactin over time and a higher prolactin level at endpoint. Thus, prolactin increase caused by low to moderate doses of haloperidol may be a correlate of endpoint symptomatology. As lower doses of typical neuroleptics are now in use, prolactin response as a predictor of clinical response may have more clinical utility. Further study of prolactin and clinical response to typical neuroleptics should focus on low neuroleptic doses.

Adult↗
PubMed1999

The secretion of prolactin in intact and lutectomized pregnant ewes. Effect of the anti-progesterone steroid RU 486.

To study the role, if any, of luteal factors in the control of prolactin secretion during the last two thirds of pregnancy in the ewe, we examined: a) the effect of RU 486 administration on prolactin secretion on days 97, 112 and 131 of pregnancy in five intact ewes and in five ewes from which the corpus luteum (CL) was removed on day 78 of pregnancy; and b) the secretory patterns of prolactin on days 60, 80, 100 and 120 of pregnancy in five intact ewes and in five ewes from which the CL was removed on day 70 of pregnancy. In a pilot experiment, we showed that daily i.v. injections (from day 91 to day 105 of pregnancy) of RU 486 at a dose of 50 mg caused a marked release of prolactin, without any effect on the secretion of progesterone and progression of pregnancy. In experiment 1, a single i.v. injection of 50 mg of RU 486 resulted in a significant (P < 0.01) increase in plasma prolactin concentrations on any day of pregnancy examined in the intact and lutectomized ewes. The prolactin responses (the maximum concentrations, the time to maximum concentrations and the area under the response curves) were not different between the two groups in any stage of pregnancy examined. In the two groups, spontaneous parturition occurred at term with alive lambs. There was no difference between the two groups in gestation length and lamb birth weight. In experiment 2, we showed that plasma concentrations of prolactin fluctuated in a pulsatile manner during the last two-thirds of pregnancy. The mean prolactin concentrations, the frequency and the amplitude of prolactin pulses were not significantly different between the intact and the lutectomized ewes in any stage of pregnancy examined. In conclusion, these experiments demonstrated that the ovine CL of pregnancy is not involved in the control of prolactin secretion in the ewe. The stimulation of prolactin secretion by the RU 486 is probably due to its anti-progesterone action exerted at the level of the receptor. The placental progesterone plays a central role in the control of prolactin secretion during the last two-thirds of pregnancy.

Animals↗
PubMed1993

Serum prolactin response to thyrotropin-releasing hormone during status epilepticus.

Determination of serum prolactin can help distinguish between epileptic and pseudo-epileptic attacks since generalized tonic-clonic and complex partial seizures frequently are accompanied by a transient rise in prolactin. In status epilepticus, however, serum prolactin levels are well within the normal range: cellular depletion due to the prolonged seizure activity has been suggested as a mechanism for this finding. The control of prolactin secretion is complex. Among several possible regulators, inhibitory dopamine and stimulatory thyrotropin-releasing hormone (TRH) may take part in the regulation of prolactin levels in connection with epileptic activity. There may be subpopulations of prolactin-producing cells that react differently in response to various regulators. A dopamine receptor blocker given during status epilepticus brings forth a distinct increase in prolactin levels. In order to add to the understanding of prolactin changes in connection with status epilepticus, we injected TRH i.v. during status epilepticus in seven consecutive patients. All patients had prolactin levels within the normal range (< 25 micrograms/l) before injection of TRH which resulted in at least a two-fold increase in prolactin levels. Our results contradict the hypothesis of cellular depletion of prolactin in connection with status epilepticus. The mechanism behind prolactin values within the normal range after prolonged seizure activity remains unknown.

Adult↗
PubMed2004

Involvement of opioid receptor subtypes in both stimulatory and inhibitory effects of the opioid peptides on prolactin secretion during pregnancy.

1. We have previously demonstrated the existence of a dual neuromodulatory regulation of prolactin secretion by the opioid system. In the present work, we evaluated the opioid receptor subtypes involved in both the stimulatory and the inhibitory regulation of prolactin secretion in pregnant rats. 2. Specific opioid agonists and antagonists were administered intracerebro ventricular (i.c.v.) to rats on day 3 and on day 19 pregnancy in rats of pretreated with mifepristone. Blood samples were obtained after decapitation at 12.00 and 18.00 h. Serum prolactin levels were measured by RIA. 3. The mu-selective agonist DAMGO and beta-endorphin caused a significant increase in serum prolactin secretion on day 3 of pregnancy, during the diurnal surge and intersurge period. Pretreatment with naloxone prevented the increase on prolactin levels induced by DAMGO. The administration of U-50,488, a kappa-selective agonist or DPDPE, a delta-selective agonist, did not modify serum prolactin concentration while the mu1-antagonist naloxonazine reduced significantly serum prolactin levels. On day 19 of pregnancy, the release of prolactin induced by mifepristone was significantly increase by naloxonazine, while the kappa-antagonist nor-binaltorfimine induced only a small but significant increase. No effect was observed after administration of the delta-antagonist naltrindole. 4. We conclude that the mu-opioid receptor seems to be more specifically involved in both the stimulatory and inhibitory regulation by the opioid system on prolactin secretion during pregnancy. The increase on serum prolactin levels on day 3 after administration of DAMGO and beta-endorphin may suggest the participation of other regulatory mechanisms as the dopaminergic and serotoninergic systems. On day 19, only the endogenous ligands delta did not participate in the regulation of prolactin secretion, while the participation of the kappa-opioid receptor was significantly less effective than the endogenous ligand mu. Our results provide evidences of an important role of the opioid system through specific receptors on the regulation of prolactin secretion during early and late pregnancy.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗