Topic
Prolactin
About: Prolactin is a research topic. Over the lifetime, 22356 publications have been published within this topic receiving 609537 citations. The topic is also known as: lactotropin, & PRL,.
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TL;DR: A new form of prolactin which has a cleavage in its large disulphide loop and is synthesised and secreted by rat pituitary glands radioactively labelled in vitro has been detected on sodium dodecyl sulphate polyacrylamide gel analysis and identified by tryptic fingerprinting.
122 citations
TL;DR: Maetz and his associates have shown that a primary osmoregulatory function of prolactin is the reduction of extrarenal sodium outflux which is uncontrolled, or poorly controlled, after removal of the hypophysis.
Abstract: THE discovery, in 1959, that prolactin enables hypophysectomized killifish (Fundulus heteroclitus) to live in fresh water1,2 stimulated much investigation of the osmoregulatory functions of this hormone in euryhaline teleosts3. The presence of prolactin, or its teleostean equivalent (paralactin), is necessary for fresh water survival in many euryhaline cyprinodonts and in some unrelated species. In others, such as the eel (Anguilla anguilla), prolactin participates less in electrolyte homeostasis, and hypophysectomized fish of such species can withstand fresh water. Maetz and his associates4–6 have shown that a primary osmoregulatory function of prolactin is the reduction of extrarenal sodium outflux which is uncontrolled, or poorly controlled, after removal of the hypophysis. This becomes critical when a prolactin-dependent species, such as F. heteroclitus, is transferred to fresh water.
122 citations
TL;DR: Evidence is presented that caveolin-1 functions as a novel suppressor of cytokine signaling in the mammary gland, akin to the SOCS family of proteins, and a similar premature lactation phenotype is observed in SOCS1 (-/-) null mice.
Abstract: It is well established that mammary gland development and lactation are tightly controlled by prolactin signaling. Binding of prolactin to its cognate receptor (Prl-R) leads to activation of the Jak-2 tyrosine kinase and the recruitment/tyrosine phosphorylation of STAT5a. However, the mechanisms for attenuating the Prl-R/Jak-2/STAT5a signaling cascade are just now being elucidated. Here, we present evidence that caveolin-1 functions as a novel suppressor of cytokine signaling in the mammary gland, akin to the SOCS family of proteins. Specifically, we show that caveolin-1 expression blocks prolactin-induced activation of a STAT5a-responsive luciferase reporter in mammary epithelial cells. Furthermore, caveolin-1 expression inhibited prolactin-induced STAT5a tyrosine phosphorylation and DNA binding activity, suggesting that caveolin-1 may negatively regulate the Jak-2 tyrosine kinase. Because the caveolin-scaffolding domain bears a striking resemblance to the SOCS pseudosubstrate domain, we examined whether Jak-2 associates with caveolin-1. In accordance with this homology, we demonstrate that Jak-2 cofractionates and coimmunoprecipitates with caveolin-1. We next tested the in vivo relevance of these findings using female Cav-1 (-/-) null mice. If caveolin-1 normally functions as a suppressor of cytokine signaling in the mammary gland, then Cav-1 null mice should show premature development of the lobuloalveolar compartment because of hyperactivation of the prolactin signaling cascade via disinhibition of Jak-2. In accordance with this prediction, Cav-1 null mice show accelerated development of the lobuloalveolar compartment, premature milk production, and hyperphosphorylation of STAT5a (pY694) at its Jak-2 phosphorylation site. In addition, the Ras-p42/44 MAPK cascade is hyper-activated. Because a similar premature lactation phenotype is observed in SOCS1 (-/-) null mice, we conclude that caveolin-1 is a novel suppressor of cytokine signaling.
122 citations
TL;DR: These experiments demonstrated a dramatic (40-fold) upregulation of prolactin (PRL) expression in TG by 17-β-estradiol (E2) and demonstrated that PRL is a novel modulator of sensory neurons tightly regulated by E2, consistent with the hypothesis thatPRL could contribute to the development of certain pain disorders.
Abstract: Sex dependency in pain perception is well documented and is thought to be attributable to the effect of reproductive hormones on nociceptive processing. In the present study, we evaluated whether estradiol alters gene transcription in the trigeminal ganglia (TG) of ovariectomized rats (OVX). These experiments demonstrated a dramatic (40-fold) upregulation of prolactin (PRL) expression in TG by 17-β-estradiol (E2). PRL expression was restricted to TG neurons and was highly overlapped with transient potential receptor vanilloid type 1 (TRPV1) (∼90%) in TG. Additionally, PRL is released from neurons during stimulation. Both forms of PRL receptors (PRLRs), short and long, were also present in TG neurons. Moreover, expression of the long PRLRs was under control of estradiol. We next evaluated the novel hypothesis that PRL acts as a neuromodulator of sensory neurons. PRL pretreatment significantly enhanced capsaicin-evoked inward currents, calcium influx, and immunoreactive calcitonin gene-related peptide release from cultured TG neurons. This PRL modulation of capsaicin responses was abolished by withdrawal of E2 from TG cultures. Biochemical analysis demonstrated that PRL increased (>50%) phosphorylation levels of TRPV1 in TG. In a behavioral test, PRL pretreatment significantly potentiated capsaicin-evoked nocifensive behavior in female rats at proestrous and in OVX rats after E2 treatment. The in vivo potentiating effect of PRL on capsaicin responses was also dependent on E2. Collectively, these data demonstrate that PRL is a novel modulator of sensory neurons tightly regulated by E2. These findings are consistent with the hypothesis that PRL could contribute to the development of certain pain disorders, possibly including those modulated by estrogen.
122 citations
TL;DR: The results demonstrate that a simple, inverse relationship between dopamine secretion and prolactin secretion does not exist during suckling, however, the observed decrease in dopamine secretion during mammary nerve stimulation may be an integral part of a complex mechanism, including other hypothalamic hormones, that lead to the release of Prolactin.
Abstract: Secretion of prolactin is tonically inhibited by hypothalamic release of dopamine into the hypophysial portal system. However, the role that changes in dopamine secretion play in altering prolactin secretion after physiologic stimuli is still unknown. The present study was designed to investigate changes in dopamine release into stalk blood during sucking-induced release of prolactin. An increase in prolactin secretion was induced in urethane-anesthetized, lactating rats by a 15-min electrical stimulation of an isolated mammary nerve trunk. This procedure induced a rapid increase in prolactin secretion, and a 7-fold increase in prolactin concentrations was observed within 20-30 min after stimulation began. In unstimulated control rats, prolactin levels remained at baseline values during the period of observation. Then, we measured the effect of this stimulus on the concentration of dopamine in hypophysial stalk plasma. Dopamine concentrations in hypophysial stalk plasma, collected at 15-min intervals before, during and after mammary nerve stimulation, decreased significantly by 20% during stimulation, returned to prestimulation values, and then increased significantly by 20% at 45-60 min. In control rats, no changes in dopamine concentrations were observed. These results demonstrate that a simple, inverse relationship between dopamine secretion and prolactin secretion does not exist during suckling. However, the observed decrease in dopamine secretion during mammary nerve stimulation may be an integral part of a complex mechanism, including other hypothalamic hormones, that lead to the release of prolactin.
122 citations