Effects of angiotensin II and natriuretic peptides of the eel on prolactin and growth hormone release in the tilapia,Oreochromis mossambicus

The effects of angiotensin II (ANG II) and natriuretic peptides (NPs) of the eel (ANP, atrial natriuretic peptide; CNP, C-type natriuretic peptide; and VNP, ventricular natriuretic peptide) on prolactin (PRL(188) and PRL(177)) and growth hormone (GH) release from the organ-cultured tilapia pituitary were examined. Eel ANG II at concentrations greater than 1 nM stimulated the release of PRL(188) and PRL(177) in a dose-related manner during the first hour of incubation. Significant stimulation by 100 nM ANG II on PRL(177) release was observed until 4h of incubation, and on PRL(188) release until 12 h. No effect of ANG II was seen on GH release. None of the NPs altered the release of PRLs at any time point. On the other hand, eel VNP at concentrations greater than 1 nM stimulated GH release in a dose-related manner after 4 h, and significant stimulation was observed until 48 h. Eel CNP was less effective than eel VNP; significant stimulation of GH release was observed at 1 and 10 nM during 24-48 h of incubation. No significant effect of eel ANP on GH release was seen at any concentration. ANG II had no effect on GH release at any time point. There was no change in mRNA levels of PRLs or GH in the pituitaries incubated with ANG II for 8 h or those incubated with the NPs for 48 h. These results indicate rapid and short-lasting stimulation by ANG II on PRL release and slow and long-lasting stimulation by VNP and CNP on GH release from the tilapia pituitary.     

Prolactin serum levels during alcohol withdrawal are associated with the severity of alcohol dependence and withdrawal symptoms

Background: Prolactin serum levels have been described to be elevated during alcohol withdrawal in alcohol‐dependent patients and normalize during abstinence. Alterations in prolactin levels may reflect disturbances of dopaminergic neurotransmission which is of crucial importance for alcohol‐seeking behavior. Methods: In this longitudinal observational study, we investigated prolactin serum levels in 99 male patients during the first 14 days of alcohol withdrawal and early abstinence and in 43 healthy controls. To assess the severity of alcohol dependence, the extent of withdrawal symptoms, craving, depressive symptoms, and anxiety, we employed a structured interview including psychologic measurements. Results: Prolactin serum levels were elevated during the whole study period in alcohol‐dependent patients compared to the healthy control group. Prolactin levels at admission (first day of alcohol withdrawal) were associated with the severity of alcohol withdrawal (CIWA‐Ar) and of alcohol dependence (SESA) but not with the other assessed psychologic parameters. Conclusions: The presented findings confirm that prolactin is significantly elevated in alcohol‐dependent patients during alcohol withdrawal and early abstinence, not showing a rapid decline after cessation of drinking. The association with the severity of withdrawal and dependence may reflect at least partially the individual alterations in the dopaminergic and glutamatergic pathways.     

A case of systemic lupus erythematosus: continued association of circulating prolactin levels with disease activity over a 4-year follow-up period

Circulating prolactin levels in a woman with systemic lupus erythematosus (SLE) were measured over a period of 4 years, and her hyperprolactinemia remained associated with disease activity throughout. Circulating prolactin could thus be a better practical marker than standard parameters such as anti-double-stranded DNA antibodies and serum complement in some patients with SLE.     

Lactation and Prolactin Release in Foster Dams Suckling Prenatally Ethanol Exposed Pups

The effect of prenatal ethanol exposure on lactation was studied employing prenatally ethanol-exposed pups transferred to foster dams following parturition. During pregnancy, from day 8 to term, dams consumed either standard laboratory chow (ad libitum control), or liquid diets containing 0%, 17.5%, or 35% ethanol derived calories (EDC). To equalize caloric intake, the 0% and 17.5% EDC groups were pair-fed to rats in 35% EDC group. Following delivery, pups born to dams fed with laboratory chow (control) or liquid diets containing 0, 17.5, or 35% EDC were adjusted to eight per litter and transferred to foster dams, which had been fed laboratory chow and water ad libitum throughout pregnancy. Foster dams were implanted with an atrial catheter on day 3 of lactation. On days 6 (early lactation) and 10 (midlactation), following separation of litters from dams for a 6-hr period, a baseline blood sample was removed via a catheter extension. Pups were weighed and returned to the dams. Subsequent blood samples were obtained 10, 30, 60, 120, and 180 min after initiation of suckling. Suckling latency and the amount of milk consumed during the 3-hr suckling were also determined. Litters were weighed on days 2, 6, 10, and 21. The prolactin surge in foster dams in response to suckling by prenatally ethanol-exposed pups was not altered on day 6 of lactation. On day 10, after the initial rise, suckling-induced prolactin was amplified in dams suckled by prenatally ethanol-exposed pups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of the estrous cycle stage on the prolactin secretory response to dopamine in vitro

Dopamine (DA) will both stimulate and inhibit prolactin (PRL) secretion from the anterior pituitary gland in vitro and in vivo. The present study was designed to determine if there are selected times during the estrous cycle of the rat when one function is favored over the other. Anterior pituitary glands collected on diestrus-1 (D1), diestrus-2 (D2), the morning of proestrus (Pro-AM), the afternoon of proestrus (Pro-PM), and estrus (E) were enzymatically dissociated and placed in monolayer culture. On the fourth day in culture, cells were challenged for 10, 20, 30, 60, 120, 180, or 240 min with media alone or media containing either 100 pM or 1 μM DA. The concentration of PRL in the media was determined by radioimmunoassay. Regression analysis revealed that in the absence of DA, PRL secretion from cultured cells differed significantly depending on the stage of the estrous cycle during which they were obtained. Cells obtained during the morning of diestrus-2 secreted PRL at the greatest rate compared to other stages of the cycle. When all stages were compared, the rates of PRL secretion were: D2>E>D1>Pro-AM>Pro-PM (each significantly different from the others,P<0.01). By 20–30 min of exposure to 100 pM DA, the rate of PRL secretion from cells obtained during each stage of the cycle was significantly enhanced. This enhanced secretion persisted in cells obtained during D2 and Pro-PM but was short-lived in cells obtained during other stages. No inhibition of PRL secretion was induced by this dose of DA. PRL secretion was inhibited when treated with 1 μM DA in cells obtained at all stages of the estrous cycle. Inhibition was more prolonged in cells obtained on D1, D2, and Pro-AM. DA was least effective as an inhibitor of PRL secretion in cells obtained during Pro-PM and E. Prior to inhibiting PRL secretion in cells obtained during Pro-PM, 1 μM DA rapidly stimulated PRL secretion. This effect persisted for 60 min. These data suggest that in the absence of DA, the dynamics of PRL secretion from anterior pituitary cells in vitro differ depending on the stage of the estrous cycle during which the cells were obtained. Moreover, the in vivo environment of the cell determines the direction and magnitude of the PRL-secretory response to DA.     

Prolactin effects on cultured pavement cell epithelia and pavement cell plus mitochondria-rich cell epithelia from freshwater rainbow trout gills

The physiological effects of ovine prolactin (oPRL) and recombinant rainbow trout prolactin (rbtPRL) on cultured gill epithelia derived from freshwater rainbow trout were assessed. Epithelia composed of either pavement cells only (single seeded inserts, SSI) or both pavement and mitochondria-rich cells (double seeded inserts, DSI) were cultured in media, supplemented with doses of oPRL ranging from 10 to 100 ng/ml. Under symmetrical culture conditions (L15 media apical/L15 media basolateral), oPRL had no effect on transepithelial resistance, paracellular permeability (assessed with PEG-4000), or Na(+) and Cl(-) transport across both preparations of cultured gill epithelia. Under asymmetrical conditions (freshwater apical/L15 media basolateral), SSI epithelia treated with oPRL (10 and 50 ng/ml), in comparison to comparably treated epithelia receiving no oPRL, exhibited a greater increase in the transepithelial resistance, particularly during the first 12h of freshwater exposure, no difference in paracellular permeability and Na(+)-K(+)-ATPase activity, and lowered net Na(+) flux rates (i.e., reduced basolateral to apical loss rates). These reflected reduced unidirectional efflux rates. The PRL effect appeared to be mainly a reduction in transcellular permeability. SSI epithelia treated with rbtPRL (10 ng/ml) exhibited similar patterns of response to those treated with oPRL. Na(+)-K(+)-ATPase activity increased in DSI epithelia treated with oPRL; however, oPRL did not stimulate ion uptake across either SSI or DSI epithelial preparations. The data demonstrated that, as the sole hormone supplement for cultured gill epithelia, PRL did not promote active ion uptake. However, the observed PRL-induced alterations in cultured gill epithelial physiology were consistent with the in vivo actions of PRL on the gills of freshwater teleost fish.     

Hormone release is tied to changes in cell size in the osmoreceptive prolactin cell of a euryhaline teleost fish, the tilapia, Oreochromis mossambicus

Prolactin (PRL) cells from a teleost fish, the tilapia, Oreochromis mossambicus, facilitate the direct study of osmoreception. The release of two prolactins, PRL(188) and PRL(177), which act in freshwater osmoregulation in teleost fish, rises in vitro within 5 min after extracellular osmolality falls. An increase in cell size accompanied this rise. Cell size and PRL release also increased, albeit more slowly, following the partial replacement of medium NaCl (55 mOsmolal) with an equivalent concentration of urea, a membrane-permeant molecule. Similar replacement using mannitol, which is membrane-impermeant, elicits no response. These findings suggest that osmoreception is linked to changes in cell volume rather than to extracellular osmolality per se.     

Prolactin-releasing peptide and its homolog RFRP-1 act in hypothalamus but not in anterior pituitary gland to stimulate stress hormone secretion

The RF-amide peptides (RFRPs), including prolactin (PRL)-releasing peptide-31 (PrRP-31) and RFRP-1, have been reported to stimulate stress hormone secretion by either direct pituitary or indirect hypothalamic actions. We examined the possible direct effects of these peptides on PRL and adrenocorticotropin (adrenocorticotropic hormone [ACTH]) release from dispersed anterior pituitary cells in culture and on PRL and ACTH secretion following intracerebroventricular (icv) administration in vivo. Neither peptide significantly altered PRL or ACTH release from cultured pituitary cells (male rat donors). Central administration of 1.0 and 3.0 nmol of PrRP-31, but only the higher dose of RFRP-1, significantly elevated serum corticosterone levels in conscious male rats. The effect of PrRP-31 was not blocked by pretreatment (iv) with the corticotropin-releasing hormone (CRH) antagonist, α-helical CRH 9–41; however, pretreatment of the animals (iv) with an antiserum to CRH significantly lowered the hypothalamic-pituitary-adrenal axis response to central administration of PrRP-31. On the other hand, the release of PRL was significantly elevated by 3.0 nmol of RFRP-1, but not PrRP-31, in similarly treated, conscious male rats. Pretreatment with the catecholamine synthesis inhibitor, α-methyl-para-tyrosine, prevented the stimulation of PRL secretion observed following central administration of RFRP-1. RFRP-1 similarly did not alter PRL secretion in rats pretreated with the dopamine, D₂ receptor blocker, domperidone. These results suggest that the RF-amide peptides are not true neuroendocrine regulators of stress hormone secretion in the rat but, instead, act centrally to alter the release of neuroendocrine factors that do act in the pituitary gland to control PRL and ACTH release. In the case of RFRP-1, stimulation of PRL secretion is potentially owing to an action of the peptide to inhibit dopamine release into the median eminence. The corticosterone secretion observed following central administration of PrRP-31 does not appear, based on our current results, to be solely owing to an action of the peptide on CRH-producing neurons but, instead, may be a result of the ability of PrRP-31 to increase as well the exposure of the corticotrophs in vivo to other ACTH secretagogues, such as oxytocin or vasopressin.