Pattern Of Prolactin Release Research Articles

Cadmium does not inhibit pulsatile prolactin secretion through TRH.

This work was undertaken to analyse the effects of acute cadmium administration on the pulsatile pattern of prolactin release, in adult male rats. For this purpose, animals were cannulated 40 h before the experiment to allow a continuous blood withdrawal. Two hours after the administration of one dose of cadmium chloride (4.5 mg kg1), the pulsatile pattern of prolactin, during three hours, was studied. The effects of two pulses of thyrotropin-releasing hormone (TRH) (1 microgram per rat), given 60 and 120 min after starting the period of blood sampling, were studied. The mean values of prolactin during the bleeding period and the absolute pulse amplitude were decreased by acute cadmium chloride administration. However, no changes in any other parameters of prolactin pulsatility were observed. TRH administration to control rats increased mean prolactin levels, and absolute and relative pulse amplitudes, but decreased the mean half-life of the hormone. In animals pretreated with cadmium, TRH increased the mean levels of prolactin, and absolute and relative amplitudes of the hormone pulses. No other parameter studied was changed by TRH in cadmium pretreated rats. These data suggest that acute administration of cadmium did not inhibit the pulsatile prolactin release through TRH.

Twenty-four hour patterns of prolactin secretion during lactation and the relationship to suckling and the resumption of fertility hi breast-feeding women

In breast-feeding women prolactin released in response to suckling is essential for the maintenance of lactation. This physiological hyperprolactinaemia is also associated with lactational infertility. However, it is not clear whether there is any direct relationship between changes in prolactin per se and the duration of infertility. To address this question, our study determined the pattern of prolactin secretion in relation to suckling and the return of ovarian activity in the same cohort of breast-feeding women. Blood samples were withdrawn at 10 min intervals for 24 h from 09:00 to 09:00 h at either 4 (n = 9) or 8 weeks (n = 11) post-partum when the women had completely suppressed ovarian activity, at the time of the introduction of supplements to the baby (n = 17), a time associated with reduction of suckling activity, at first menses while still breast-feeding (n = 13) and in the follicular phase (n = 9) of the first menstrual cycle after weaning. During sampling, mothers and babies continued their normal pattern of suckling activity. The pattern of prolactin release was very variable at each stage of lactation, depending on the pattern of suckling. Frequent suckling was associated with elevated prolactin concentrations during the 24 h period throughout lactation. When suckling was less frequent, prolactin concentrations fell to baseline values between breast-feeds, but prolactin was released in response to all suckling episodes. An increase in prolactin concentrations at night, independent of suckling, was only evident once breast-feeding had ceased. The prolactin response to suckling declined significantly only after the return of menses at 33.6 +/- 3.5 weeks post-partum. There was no relationship between the duration of amenorrhoea and the plasma concentrations of prolactin over 24 h, or day or night separately, throughout lactation. However, there was a strong correlation (r = 0.843; P < 0.01) between the timing of the introduction of dietary supplements to the baby and the duration of amenorrhoea. These results suggest that there may be no precise link between the release of prolactin during lactation and the duration of lactational infertility in breast-feeding women.

Somatostatin partially impedes the stimulatory effects of thyrotrophin-releasing hormone and dibutyryl cyclic AMP on prolactin release: prolactin release through multiple routes

Patterns of prolactin release were examined using stimulating and inhibiting agents. Primary cultured pituitary cells primed with oestrogens were used for perifusion experiments. TRH (100 nmol/l) increased the peak prolactin concentration to 360% of the basal concentration, while TRH, under inhibition by 1 nmol somatostatin/l, raised the peak prolactin concentration to 185% of the basal levels. When the somatostatin concentration was increased to 10, 100 and 1000 nmol/l, TRH still stimulated prolactin release to 128%, 121% and 140% respectively, indicating that concentrations of somatostatin of 10 nmol/l or higher did not further suppress the stimulatory effect of TRH. TRH (1 mumol/l) stimulated prolactin release under the influence of 0 (control), 1, 10, 100 and 1000 nmol dopamine/l (plus 0.1 mmol ascorbic acid/l) to 394, 394, 241, 73 and 68% of the basal concentration respectively, showing that the dopamine concentrations and peak prolactin concentrations induced by TRH have an inverse linear relationship in the range 1-100 nmol dopamine/l. The stimulatory effect of dibutyryl cyclic AMP (dbcAMP) on prolactin release was also tested. The relationship between dbcAMP and somatostatin was similar to that between TRH and somatostatin. When adenohypophyses of male rats were used for perifusion experiments, somatostatin (100 nmol/l) did not inhibit basal prolactin release from the fresh male pituitary in contrast with the primary cultured pituitary cells, but dopamine (1 mumol/l) effectively inhibited prolactin release. In conclusion, (1) oestrogen converts the somatostatin-insensitive route into a somatostatin-sensitive route for basal prolactin release, (2) TRH-induced prolactin release passes through both somatostatin-sensitive and -insensitive routes, (3) dopamine blocks both somatostatin-sensitive and -insensitive routes and (4) cAMP activates both somatostatin-sensitive and -insensitive routes.

Attenuation of the Suckling-Induced Prolactin Release and the High Afternoon Oscillations of Plasma Prolactin Secretion of Lactating Rats by Antiserum to Vasopressin

To investigate the role of vasopressin in prolactin (PRL) release during lactation, vasopressin antiserum (VP-Ab) was administered to lactating rats, giving it intravenously 15 min before permitting their previously isolated pups to suckle or to continuously suckled rats. The suckling-induced rise in plasma PRL levels was significantly less in VP-Ab-treated mothers than in rats receiving a similar amount of normal rabbit serum (NRS). The inhibitory effect of VP-Ab could not be detected on the next day. Angiotensin II antiserum (AII-Ab) had no effect on plasma PRL response induced by suckling. VP-Ab given to continuously suckled rats reduced the high amplitude oscillation of PRL concentration observed in NRS-injected rats. A transient increase of water intake was detected on the day of VP-Ab treatment only, which provides direct evidence for at least partial neutralization of vasopressin in the circulation. These findings suggest that vasopressin released from the neural lobe of the pituitary gland is essential for the normal PRL secretory response induced by suckling and the episodic pattern of PRL release in continuously suckled mother rats. Furthermore, these results support the assumption that disturbance in the regulation of water and electrolyte balance at the level of the neuro-intermediate lobe of the pituitary gland may alter PRL secretion during lactation.

The patterns of prolactin release by ECT and TRH compared

The patterns of prolactin release after bilateral ECT and after 0.4 mg TRH i.v. were studied in 11 female melancholic patients in a 5-min sampling protocol. Mean prolactin peaking times were 10.2 min after ECT and 20.5 min after TRH. The elimination rate coefficients were significantly lower - and the corresponding half-lives longer - for prolactin released by TRH than by ECT. A significant posive correlation of the maximal prolactin responses by the two stimuli was also found.

Effects of sequential acute stress exposure on stress-induced pituitary luteinizing hormone and prolactin secretion

The present study was carried out to determine the effects of repetitive acute stress exposure on pituitary secretion of both luteinizing hormone (LH) and prolactin (PRL). Adult male rats were exposed to sequential episodes of acute novel environment stress separated by intervals of either 60 or 120 minutes. Serial blood samples were obtained from animals before, during and after each stress episode via indwelling intra-cardiac cannulas. The imposition of 10 minute episodes of novel environment stress on an hourly basis eventually rendered the hypothalamic-hypophyseal LH axis refractory to the stimulatory effect of stress. If sequential stress was imposed at 120 minute intervals, LH release was significantly enhanced during each exposure. A different pattern of PRL release was observed during the same sequential stress schedule. After an initial increase in hormone release in response to the first hourly stress episode, PRL levels were unaltered during the second and third hourly stress exposures. Thereafter, plasma PRL levels showed a trend toward a progressive increase in release during each successive episode, and were significantly elevated above preceding baseline levels during the fourth and fifth hourly stress exposures. In rats exposed to stress every two hours, a significant increase in PRL levels occurred following the first, but not the second stress episode. Hormone release was again enhanced in response to the third exposure to novel environment. The present results demonstrate that the repetitive exposure to acute novel environment stress results in differential alterations in pituitary LH and PRL secretion over time, and that the timing of repeated episodes is an important determinant of continued responsiveness to stress, particularly with regard to LH release. These findings suggest that the LH and PRL hormonal responses to at least this specific stressor are mediated by independent neural mechanisms.

Prolactin-releasing effect of zetidoline, a new neuroleptic agent, in the rat

The effect of a new neuroleptic agent, zetidoline, 1-(3-chlorophenyl)-3-[2-(3,3-dimethyl-l-azetidinyl)ethyl]imidaz olidin-2-one (ZET), on prolactin release was studied in both male and female rats and compared to that of the classic antipsychotic drugs chlorpromazine and haloperidol. Time-course and dose-effect studies showed that ZET induces a rapid and short lasting increase in plasma prolactin levels, with a significant increase after a dose as low as 0.33 mg/kg, i.p.. The overall patterns of prolactin release appeared to be similar in both sexes but the response was markedly greater in females than in males. The prolactin-releasing effect of ZET was counteracted by apomorphine and L-dopa, which indicates that blockade of dopamine receptors is the basis of its neuroendocrine action. As a prolactin-releaser, ZET was found to be about 5 times as potent as chlorpromazine and about one-ninth as potent as haloperidol.

Isolated prolactin and growth hormone granules from bovine pituitary: content and stability are seasonally dependent.

Secretory granules containing prolactin (PRL) and growth hormone (GH) as essentially the only proteins were isolated by centrifugation. PRL and GH varied reciprocally in the granule preparations with the seasons. During winter PRL content was lowest (20%) and GH highest (80%); during summer the converse obtained: PRL, 70% and GH,, 30%. Both hormones were in almost equal proportion during the spring. The amount of either hormone released from granules and pituitary slices was directly related to its relative content in the gland. The pattern of PRL release from secretory granules and pituitary tissue in vitro was similar to that reported for blood levels in ruminants: low during winter and high during summer. It is concluded that seasonal factors affect primarily the synthesis and/or storage of PRL and GH, and there exists a direct relationship between intracellular stores and release.

On the control of prolactin and growth hormone synthesis in rat pituitary glands.

Pituitary gland prolactin and growth hormone content are decreased in rats bearing certain hormone-secreting pituitary tumors. The present study shows that this is the result of decreased hormone synthesis and not increased release of pituitary gland hormones. Pituitary glands were incubated in vitro in tissue culture Medium 199 containing leucine-4,5-3H. Aliquots from pituitary gland homogenates and incubation medium were subjected to polyacrylamide gel electrophoresis and the optical density and radioactivity in the protein bands measured. The synthesis of hormones was observed for varying time periods up to 21 hr. Labeled prolactin appears in the medium promptly and is not retained in the gland, whereas growth hormone is largely retained in the gland. Both hormones are synthesized at comparable rates. Glands from rats with tumors MtTW5, StW5 or 7315a synthesized prolactin at a rate approximately 50% that found in control glands. No change in the pattern of prolactin release was found in glands from tum...