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PubMed1995

Effects of remoxipride and raclopride on prolactin release from clonal pituitary tumour cells.

The dopamine D2 receptor antagonist remoxipride (30 microM) stimulated prolactin release from the prolactin-producing rat pituitary tumour cell strains GH3 and GH4C1 as well as from transfected GH4C1 cells expressing the short isoform of the rat D2 receptor (GH4ZR7). The effect of remoxipride on prolactin release is probably not due to an interaction with D2 receptors since GH4C1 cells, in contrast to GH3 and GH4ZR7 cells, are completely devoid of D2 receptors; in contrast, we have previously shown that the D2 antagonist haloperidol causes prolactin release from D2 receptor-expressing cells, only. Exposure of GH3 cells to the inhibitor of intracellular Ca2+ mobilization, 8-(diethylamino)-octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8) prevented the prolactin-releasing effect of remoxipride whereas pretreatment with the membrane Ca2+ channel antagonist nimodipine did not influence the response. The D2 receptor antagonist raclopride counteracted the reduction of VIP-stimulated prolactin release induced by the D2 agonist quinpirole but caused no prolactin release per se.

Animals↗
PubMed1986

Effects of timed melatonin infusion on prolactin secretion in pineal denervated goat.

The effects of timed melatonin infusion on prolactin secretion were examined in the pineal denervated goat. Ovariectomized Shiba goats (n = 5) were subjected to bilateral superior cervical ganglionectomy (SCGX); this procedure resulted in complete abolition of endogenous melatonin release during the dark phase. SCGX goats failed to coordinate their prolactin secretion with the prevailing photoperiod. Melatonin was infused (20 micrograms/h, s.c.) daily into these goats either for 8 h (the long-day-type infusion) or for 16 h (the short-day-type infusion) to mimic the nocturnal profile of plasma melatonin under long days or short days, respectively. The long-day-type melatonin infusion for 9 days, in comparison with control saline infusion, accelerated prolactin secretion, inducing a nocturnal rise in plasma prolactin; this was comparable to that seen in the pineal intact goats under long photoperiods. On the other hand, the short-day-type melatonin infusion suppressed prolactin secretion throughout the day as the short-day treatment did in intact goats. The prevailing photoperiod appeared to have no distinct effect on these prolactin responses to exogenous melatonin, which were indistinguishable under 16L8D and 8L16D conditions. The results indicate that the information about external light-dark cycles is converted by the pineal gland into the endocrine signal as a daily pattern of melatonin secretion, which eventually regulates prolactin secretion from the pituitary gland of the goat.

Animals↗
PubMed1983

Plasma prolactin levels and body fluid deficits in the rat: causal interactions and control of water intake.

A study was made of the responses of chronically hyperprolactinaemic rats to selected dipsogenic stimuli. Measurements were also made of the correlation between the state of hydration of the animal and the plasma prolactin levels. After 24 h water deprivation. S.C. isoprenaline (10 micrograms/kg body wt.) or I.P. injection (5 ml/kg body wt.) of a hypertonic solution (50% w/w) of polyethylene glycol (mol. wt 20000) there was no difference between the hyperprolactinaemic and control rats with respect to the total water intake, the time course of drinking or the urine output. After I.V. injection of 2 M-NaCl (5 ml/kg body wt.) there was no difference between the hyperprolactinaemic and control rats with respect to the total water intake or urine output. However, the hyperprolactinaemic rats drank more slowly than the controls. When angiotensin II was infused I.V. at a rate of 0.2 micrograms/min, the water intake was greater and the threshold to drinking lower in the hyperprolactinaemic than control rats. After 24 h water deprivation, plasma prolactin levels rose significantly in both the control and hyperprolactinaemic rats. When the rats were injected I.V. with hypertonic saline (5 ml, 2 M-NaCl/kg body wt.) and denied access to water, plasma prolactin levels had not changed 1 h later in either the control or hyperprolactinaemic animals. It is concluded that there is no interaction either between the plasma osmolality and prolactin secretion or between the plasma prolactin levels and the amount of water drunk in response to intracellular fluid deficits. However, prolactin secretion is stimulated by the combined intra- and extracellular deficits resulting from water deprivation and there is a clearly demonstrated interaction between prolactin and the extracellularly mediated stimulus of angiotensin II.

Angiotensin II↗
PubMed1974

Actions of prolactin and frusemide on heart rate and rhythm.

Rat hearts with coronary circulations perfused by the Langendorff technique were studied. Recordings were made of the electrical and mechanical activity. Once the rate and rhythm of each heart and stabilized it was perfused with Ringer-Locke solution for 90 minutes; frusemide (40 mug/ml) was added to the perfusate during the last 30 minutes of this period. Eighteen experiments were performed-six controls, six in which prolactin at a concentration of 50 ng/ml was added to the perfusate for the whole 90 minutes, and six in which a prolactin concentration of 200 ng/ml was used.With the controls heart rate and rhythm remained steady, but there was a slow decline in amplitude of the contraction. With a prolactin concentration of 50 ng/ml the heart rate rose to about 40% above control during the first hour and after an initial sharp increase the contraction amplitude declined more rapidly than in the controls. The prolactin concentration of 200 ng/ml produced a decline of about 25% in heart rate over the first hour and amplitude behaved much as in the controls. Frusemide had no clear effect on the rate of beating of the controls, but it tended to reverse both the acceleration produced by 50 ng/ml prolactin and the slowing produced by the higher dose. Both the doses of prolactin consistently caused disturbances of rhythm. These effects occur at concentration of prolactin found in human plasma in various pathophysiological conditions.

Animals↗
PubMed1992

Serum prolactin response to metoclopramide during status epilepticus.

Transient elevation of serum prolactin frequently follows generalised tonic-clonic and complex partial seizures. However, the levels of prolactin during status epilepticus are not increased above the normal range. Exhaustion of central prolactin supplies has been proposed as a possible mechanism for the absence of prolactin increase during status epilepticus. To test this hypothesis we injected intravenous metoclopramide (10 mg) in eight consecutive patients with status epilepticus. One patient had generalised tonic-clonic status epilepticus. Seven patients had EEG-verified non-convulsive status epilepticus, consisting of one typical absence status, one atypical absence status and five complex partial status epilepticus. Metoclopramide raised the mean (SD) prolactin levels at least five-fold in all patients, from 5.8 (8.0) micrograms/l to 87.0 (39.0) micrograms/l, within 60 minutes after the injection. Thus the mechanism for low prolactin values in status epilepticus is not cellular depletion of stored prolactin, but more likely an altered regulation, presumably induced by prolonged seizure activity.

Aged↗
PubMed1995

Serum prolactin concentration in pseudopregnant and normally reproducing goats.

Previous experiments with bromocriptine suggested that prolactin plays a role in the aetiology of pseudopregnancy in goats. Serum prolactin concentration was measured in a herd of white Dutch dairy (Saanen) goats when hydrometra (a typical characteristic of pseudopregnancy) was diagnosed by ultrasound, during the spontaneous development of pseudopregnancy, and in normally reproducing goats during the breeding season. In the normally reproducing does the prolactin concentration decreased at the beginning of the breeding season. In 12 of 14 pseudopregnant goats the prolactin concentration was within the range observed in the normally reproducing goats on the day that hydrometra was diagnosed. In two goats the prolactin concentration was low during the first few weeks of pseudopregnancy and in a third it fluctuated. There was no correlation found between the concentration of prolactin and the development or the presence of a persistent corpus luteum. These results suggest that prolactin does not play a crucial role in the aetiology of pseudopregnancy in the goat.

Anestrus↗
PubMed1977

Influence of infused prolactin on hormone binding to tissue slices.

The influence of circulating prolactin on the binding of labeled hormone to tissue slices in vitro was investigated in rats bearing dimethylbenzanthracene-induced mammary tumors. Prolactin was infused into four animals over four 30-min periods to give serum levels ranging from 20 to 2000 ng/ml. Serial biopsies of liver and tumor were taken during infusion, and binding of labeled prolactin and insulin measured in tissue slices. Whereas insulin binding remained constant, prolactin binding was significantly depressed in both tissues when samples were obtained at serum prolactin levels greater than 300 ng/ml. This decrease was due to diminished numbers of available binding sites rather than a change in binding-site affinity for prolactin. The data indicate that under the conditions of this experiment, endogenous circulating prolactin may interfere with in vitro measurements of hormone uptake when serum levels excee 300 ng/ml.

Animals↗
PubMed1978

Hypothalamic catecholaminergic effects on prolactin release in vitro.

Hypothalamic catecholaminergic influences on prolactin release were investigated in vitro. Both dopamine and norepinephrine caused long lasting inhibition of prolactin release from either an isolated hemipituitary or a hemipituitary coincubated with a hypothalamus. Epinephrine also inhibited prolactin release. L-Dihydroxyphenylalanine (L-dopa) inhibited prolactin release from pituitaries in the presence of a hypothalamus but not in isolated pituitaries. DL-Threodihydroxyphenylserine (threodops), serotonin, 5-hydroxy-L-tryptophan (5-HTP), tyramine, octopamine, synephrine, thyrotropin-releasing hormone (TRH), luteinizing hormone releasing hormone (LH-RH), and somatostatin all failed to alter prolactin release. Results confirm that dopamine and norepinephrine directly inhibit prolactin release from pituitary and suggest that the hypothalamic mechanism inhibiting prolactin involves dopamine but not norepinephrine.

Animals↗
PubMed1984

Evidence that cobalt ion inhibition of prolactin secretion occurs at an intracellular locus.

Cobalt inhibition of stimulated prolactin secretion has been interpreted as demonstrating an essential role for enhanced calcium influx in the action of thyrotropin-releasing hormone (TRH) in GH3 cells. However, this interpretation is based on the assumption that cobalt ion (Co2+) binds to the external surface of cells to antagonize calcium-mediated processes only by blocking influx of extracellular calcium ion (Ca2+). In this report, we present evidence that Co2+ acts at an intracellular locus (or loci) to inhibit prolactin secretion. When GH3 cells were incubated in medium containing 1.5 mM Ca2+, Co2+ inhibited basal as well as 50 mM K+- and TRH-induced secretion; half-maximal effect occurred between 0.1 and 0.3 mM Co2+. When cells were incubated in medium containing 0.05 and 0.003 mM Ca2+, concentrations that abolish 50 mM K+-induced prolactin secretion, Co2+ still inhibited basal and TRH-stimulated prolactin secretion. Co2+ also inhibited prolactin secretion stimulated by 1-methyl-3-isobutylxanthine, dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP), and vasoactive intestinal peptide, three secretagogues that act to elevate intracellular cAMP, a mechanism which appears not to involve enhanced Ca2+ influx. Last, the presence of Co2+ within the cell was shown by fluorescence quenching of intracellularly trapped Quin 2, a chelator of divalent cations. These data demonstrate that Co2+ enters GH3 cells and that Co2+ inhibition of prolactin secretion does not involve extracellular Ca2+. We suggest that Co2+ not only blocks Ca2+ channels in GH3 cells, but it inhibits prolactin secretion at an intracellular locus (loci). Hence, inhibition by Co2+ should not be interpreted as demonstrating a requirement for Ca2+ influx in stimulated secretion.

Animals↗
PubMed1981

Transepithelial electrophysiology of cultured mouse mammary epithelium: sensitivity to prolactins.

Several prolactins and growth hormones affect cultured BALB/c mouse mammary epithelial electrophysiology at doses of 10 micrograms/ml. Ovine prolactin is effective at doses as low as 1 ng/ml, levels that are three to four orders of magnitude less than effective amounts of rat growth hormone. Because growth hormone preparations may have approximately 1% prolactin contamination, its effects are probably due to prolactin contamination. The maximum effect of ovine prolactin on short-circuit current and on resistance occurs at doses differing by two orders of magnitude, indicating that these two effects of prolactin may be partially separable. Therefore, prolactin may have effects on passive permeability properties in addition to its documented effects on active transport.

Animals↗
PubMed1986

Estradiol induces a shift in cultured cells that release prolactin or growth hormone.

The process by which estradiol induces an increase in the percentage of prolactin cells in the rat pituitary requires clarification. In this study the effect of estradiol treatment on growth hormone and prolactin cells in monolayer cultures of male rat pituitaries was assessed by use of reverse hemolytic plaque assays. Treatment of cultures with 17 beta-estradiol (10 nM) for 6 days elevated significantly (P less than 0.01) the percentage of all cells in culture that released prolactin without affecting the percentage of growth hormone secretors. However, by sequentially assaying single cells for growth hormone and prolactin, we found that estradiol caused a marked increase (P less than 0.01) in the proportion of individual cells that released both growth hormone and prolactin and a commensurate decrease in the proportion that released growth hormone alone. These results demonstrate that estradiol acts directly on cultures of male pituitary cells to shift the proportions of cells that released growth hormone, prolactin, or both hormones and indicate that estradiol may convert cells that release only growth hormone to those that release both growth hormone and prolactin.

Animals↗
PubMed1990

Tumor necrosis factor-alpha and interferon-gamma reduce prolactin release in vitro.

Prolactin binds to lymphocytes and monocytes and can modulate immune cell function. It was postulated that proteins released from activated macrophages and lymphocytes could directly influence prolactin release and thus form an endocrine control loop during infection, tumor invasion, or inflammation. This hypothesis was tested by exposing cultured rat anterior pituitary cells to murine tumor necrosis factor-alpha (TNF-alpha) and/or interferon-gamma (IFN-gamma) for 24 h before a 4-h test of cell function. Overall prolactin accumulation during this first 24 h was inhibited by TNF-alpha and markedly reduced by TNF-alpha plus IFN-gamma. In contrast, thyroid-stimulating hormone levels were unchanged in these same media. During the subsequent 4-h challenge, both cytokines reduced thyrotropin-releasing hormone-stimulated prolactin release but had no effect on inhibited prolactin release mediated by dopamine and somatostatin receptors. Cellular viability (assessed by trypan blue and chromium release assays) and prolactin cell content were unchanged after TNF-alpha or IFN-gamma treatment. We conclude that both TNF-alpha and IFN-gamma have the potential to act directly on anterior pituitary cells to slow the rate of prolactin release.

Animals↗
PubMed1989

Prolactin stimulates food intake in a dose-dependent manner.

Lactation in the rat is marked by pronounced hyperphagia and suppression of brown fat (BAT) thermogenic capacity. We previously examined the possibility that elevated prolactin levels mediate these changes. The present study evaluated the effect of varying prolactin levels on food intake, BAT mitochondrial GDP binding, and carcass adiposity. Female rats were injected daily for 10 days with ovine prolactin at one of three doses: high = 3.0, medium = 1.0, or low = 0.3 micrograms/g body wt. Controls were injected with 0.9% NaCl. A group of uninjected rats served as an additional control. Cumulative food intake was significantly elevated in a dose-dependent manner in the prolactin-treated animals relative to the saline-injected and uninjected controls. Compared with the saline controls, the mean cumulative food intake was greatest at the high dose (20% increase), intermediate at the medium dose (17%), and smallest at the low dose (12%). Prolactin-treated rats gained significantly more weight during the experiment than did controls. Despite the hyperphagia in the prolactin-treated rats, no significant differences in BAT mitochondrial GDP binding were observed among the five groups. These data indicate that elevated prolactin levels stimulate food intake in a dose-dependent manner and that this hyperphagia is not accompanied by an increase in BAT mitochondrial GDP binding.

Adipose Tissue↗
PubMed1989

Exercise training and the differential prolactin response in male and female rats.

Adult male and female Sprague-Dawley rats were trained on a horizontal treadmill for 0, 1, 3, 5, or 7 days/wk for 10 wk. Speed and duration were progressively increased over 5 wk to a maximum of 20 m/min for 1 h. Between weeks 9 and 10 of training, animals were placed on the nonmoving treadmill, and blood (500 microliters) was sampled via chronic venous cannulas 30 min before, 0, 10, 20, 30, 45, and 60 min during exercise, and 15, 30, 60, 90, and 120 min after exercise. In another study, resting animals in the various groups were injected with thyrotropin-releasing hormone (TRH; 2 micrograms/kg for males and 0.4 microgram/kg for females) to determine pituitary prolactin responsiveness. In males, exercise induced a significant increase in plasma prolactin levels, with the greatest increase observed in the least trained and the smallest increase in the most highly trained animals. Female rats displayed the opposite trend with the greatest increase in prolactin secretion observed in the highest trained and the smallest increase observed in the least trained animals. TRH induced similar increases in plasma prolactin in all male groups, whereas TRH-induced prolactin release was greatest in the highest trained and smallest in the least trained females. The reduced prolactin response in highly trained males may reflect their acclimation to repetitive exercise stress, whereas the enhanced response in the highly trained female rats appears to result from increased pituitary sensitivity to prolactin-releasing factors.

Animals↗
PubMed1991

Adrenal activation and the prolactin response to exercise in eumenorrheic and amenorrheic runners.

Adrenocorticotropic hormone (ACTH), cortisol, and prolactin responses following maximal and submaximal (40 min at 80% maximal O2 consumption) running were studied in eumenorrheic (ER; n = 8, 29.0 +/- 1.5 yr) and amenorrheic (AR; n = 8, 24.5 +/- 2.0 yr) runners. ER were studied in the early follicular and midluteal phases of the menstrual cycle. Physical, training, and gynecological characteristics were similar, and cardiorespiratory and metabolic responses to the exercises were indistinguishable in the groups. ACTH, cortisol, and prolactin data from the follicular luteal phases in ER were combined for comparison to AR, because no differences were noted between the menstrual phases at rest. Similar preexercise ACTH levels and responses following exercise occurred in both groups, but preexercise cortisol levels were elevated (ER = 293.1 +/- 46.3, AR = 479.6 +/- 42.4 nmol/l) and cortisol responses blunted in AR. Adrenal sensitivity was blunted in AR compared with ER after submaximal (ER = 121.9 +/- 17.4, AR = 51.7 +/- 13.6) and maximal exercise (ER = 27.9 +/- 9.2, AR = 12.1 +/- 3.8). Preexercise prolactin levels were reduced (ER = 16.4 +/- 2.7, AR = 10 +/- 2.3 micrograms/l), and prolactin responses to maximal exercises were blunted in AR, despite high lactate levels (11.4 +/- 0.4 mmol/l). We conclude that 1) control for menstrual phase in ER is important in studies of prolactin responses following exercise but not in studies of ACTH and cortisol responses following exercise, 2) cortisol responses following submaximal and maximal exercise in AR are blunted at the adrenal level, 3) prolactin responses following submaximal and maximal exercise are also blunted in AR, and 4) prolactin responses following exercise may be mediated by adrenal activation.

Adolescent↗
PubMedDate not supplied

Prolactin levels of fathers and helpers related to alloparental care in common marmosets, Callithrix jacchus.

Previous studies have suggested that prolactin may play a role in regulating allocare behaviour in cotton-top tamarins, Saguinus oedipus. In this study, we investigate the prolactin profile of 3 groups of captive common marmosets, Callithrix jacchus. Carrying behaviour in this species was observed after parturition. Prolactin assays of blood samples of both fathers and helpers (sub-adult non-fathers) in 3 family groups were taken for 8 weeks before and after birth of the infants. The after-birth condition was divided into 2 groups: carrying and non-carrying animals. The results suggest a relationship between prolactin levels and allocare behaviour, with carrying behaviour being associated with increased prolactin in both fathers and helpers. This suggests that extra prolactin is produced in response to physical contact, and may be associated with carrying behaviour. Also, prolactin production may be related to learning parental skills in Neotropical primates.

Animals↗
PubMed2000

Immunoneutralization of endogenous opioid peptides prevents the suckling-induced prolactin increase and the inhibition of tuberoinfundibular dopaminergic neurons.

Previous studies have shown that the endogenous opioid peptides, acting at specific opiate receptor subtypes, are involved in the suckling-induced prolactin secretory response. The prolactin increase elicited by suckling is due, at least in part, to an inhibition of tuberoinfundibular dopaminergic (TIDA) neurons in the hypothalamus. We investigated the effects of immunoneutralization of dynorphin, leu-enkephalin and met-enkephalin on the suckling-induced prolactin increase and on the activity of the TIDA neurons in lactating female rats between days 7 and 12 postpartum. Rats were injected into the right lateral ventricle with antiserum specific for one of these three peptides. Control rats were administered equal amounts of immunoglobulin proteins. Suckling produced a profound and significant increase in prolactin levels, as well as a decrease in DOPA accumulation in the median eminence of lactating rats. Administration of immunoglobulin concentrations of up to 3.6 microg did not inhibit the prolactin secretory response to the suckling stimulus and did not prevent the suckling-induced inhibition of TIDA neurons. Antisera to all three endogenous opioid peptides abolished the suckling-induced prolactin increase and prevented the inhibition in DOPA accumulation in the median eminence. Thus, the endogenous opioid peptides, dynorphin, leu-enkephalin and met-enkephalin, are essential for the prolactin secretory response to suckling and inhibition of TIDA neuronal activity is at least one of the mechanisms of action utilized by these peptides.

Animals↗
PubMed1979

Immobilization stress and prolactin secretion in male rats. Possible roles of dopamine and TRH.

Immoblization stress had a biphasic effect on serum prolactin levels: the early short stimulatory phase followed by a long inhibitory phase in male rats. Stress induced the rise in serum prolactin without concomitant increase in serum TSH levels which declined during the immoblization for 300 min. Other stressors, ether inhalation or formalin s.c. injection, or TSH i.v. injection, which were effective in controls failed to elevate serum prolactin after the 300-min immobilization. Serum TSH responded to TRH after the stress as well. Pimozide, dopamine receptor blocker, was effective in increase of serum prolactin in the stressed rats as well as in controls. In pimozide pretreated rats, elevated serum prolactin levels decrease in 10 min by the immobilization and returned to the preimmobilization levels thereafter which were higher than those in stressed animals without pimozide treatment. It is suggested that TRH is not a physiological PRF in the stress-induced prolactin release and that the dopaminergic system may be activated by the immunoblization stress, resulting in decrease of the prolactin-releasing activity of the pituitary.

Animals↗