Modulation of anterior pituitary dopamine receptors by estradiol 17‐β: Dose‐response relationship

Ali, Syed F.; Peck, Ernest J.

doi:10.1002/jnr.490130404

Cited by 22 publications

(6 citation statements)

References 18 publications

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“…The latter observation is in agreement with the report that transplanted cells are more sensitive to secretagogues (24) and because DA is more effective inhibiting newly synthetized PRL (25). The data obtained from in vitro responsiveness of PRL to DA of in situ pituitaries from sham-operated animals, previously treated with CyA, suggests that changes induced in plasma oestradiol levels as were shown previously (5) may be involved in the the drug effects on the pituitary, changing the number of receptors for DA on the lactotrophs (26,27,28). Therefore, the previous endocrine milieu, induced by the treatment with CyA, directly influences the in vitro pituitary responsiveness to external stimuli as was described previously (29).…”

Section: Discussionsupporting

confidence: 91%

Cyclosporine Effects on in vitro Responsiveness of Anterior Pituitary Hormone Release to Dopamine and Thyrotropin‐Releasing Hormone in Young Female Rats

Arce

et al. 1995

J Neuroendocrinology

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Endocrine side effects of the immunosuppressive drug cyclosporine (CyA) include changes in anterior pituitary hormone secretion. The aim of the present study was to examine the effects of CyA on the responsiveness of in situ and ectopic anterior pituitary prolactin (PRL), growth hormone (GH) and luteinizing hormone (LH) release response to dopamine (DA) and thyrotropin-releasing hormone (TRH) treatment in young female rats, and to evaluate the possible PRL participation in these effects. Thirty day old rats were rendered hyperprolactinemic by transplanting an anterior pituitary gland of a littermate donor, under the kidney capsule, and were then injected with CyA or vehicle for 2 or 8 days. Sham-operated rats were used as controls and treated in the same way. CyA treatment prevented the increase in plasma PRL levels which occurred in controls after pituitary grafting. In vitro basal PRL release of in situ pituitaries from either sham-operated and/or pituitary-grafted animals was decreased by CyA treatment at any point studied. Basal in vitro secretion of GH was only decreased in the in situ pituitaries from grafted animals after 2 days of CyA therapy. The presence of an ectopic pituitary lead to an increase in the in vitro basal LH secretion from in situ pituitaries as compared to those from sham-operated rats. Basal LH release rates were not changed by CyA treatment, although the LH release in vitro did increase in the in situ pituitaries from sham-operated animals treated with the drug for 2 days. DA addition to the incubation media decreased the in vitro release of PRL, GH and LH from the in situ pituitaries of sham-operated and pituitary-grafted animals treated with vehicle. In CyA treated animals, DA decreased in vitro PRL release from the in situ pituitaries of animals, independently of the presence or absence of an ectopic pituitary. Reductions of the in vitro GH and LH release release after DA treatment were higher in the in situ pituitaries from grafted animals on day 8 of CyA or vehicle treatment. TRH increased the in vitro release of the three hormones with differential effects related to the length of the treatment with CyA and/or the presence of an ectopic pituitary. In vitro release of PRL and GH by ectopic pituitaries was inhibited by previous treatment with CyA and this effect was decreased proportional to the duration of the treatment with the drug, while LH secretion was not modified. Addition of DA to the incubation media resulted in a marked reduction of in vitro PRL and GH release, but only at day 8 of vehicle treatment on GH release did DA addition to media further decrease the release of both hormones from ectopic pituitaries from animals treated for 2 or 8 days with the drug, whereas LH secretion was not modified. TRH addition to the incubation media of ectopic pituitaries surprisingly reduced PRL and GH secretion on day 8 of CyA treatment or after surgery. The results of these studies suggest that CyA can act directly at the hypophyseal level modifying pituitary responsiveness to external...

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Section: Discussionsupporting

confidence: 91%

Cyclosporine Effects on in vitro Responsiveness of Anterior Pituitary Hormone Release to Dopamine and Thyrotropin‐Releasing Hormone in Young Female Rats

Arce

et al. 1995

J Neuroendocrinology

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“…Acute effects of 178estradiol have also been shown in GH, cells (31,32). The present results, obtained by perifusion and RHPA cannot preclude the possibility of short-term effects by 178-estradio1, and what is more they contradict other reports which indicate that 48 h treatment is necessary to show the effects of 17P-estradiol (30). However, it has been shown that estrogen acts in different tissues with varying latencies ranging from seconds and minutes to hours and days (33), and it is unlikely that a single mechanism of action is involved.…”

Section: Discussioncontrasting

confidence: 79%

“…Consequently, a certain number of cells which may be sensitive to DA could possibly have previously liberated sufficient hormone to be classed as large plaque-forming cells, and thus falsify the data. 178-estradiol effects on DA receptors in lactotrophs from ovariectomized female rats have been shown to have different times of action; acute (several minutes) (6) or chronic (several hours) (30). Acute effects of 178estradiol have also been shown in GH, cells (31,32).…”

Section: Discussionmentioning

confidence: 99%

In vitro Effects of 17Beta‐Estradiol on Thyrotropin‐Releasing Hormone‐Induced and Dopamine‐lnhibited Prolactin Release from Adult Male Rat Lactotrophs in Primary Culture

Zhang

Chen

Kukstas

et al. 1990

J Neuroendocrinology

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Continuous cell perifusion and reverse hemolytic plaque assay have been used to show a regulatory action of 178-estradiol on lactotroph responsiveness to thyrotropin-releasing hormone (TRH) or dopamine (DA) in vifro. Lactotroph-enriched cell cultures were obtained from adult male rats after trypsinization and mechanical dissociation followed by separation on a continuous bovine Serum albumin gradient at unit gravity. After 7 days in culture, perifusion experiments showed that prolactin was continuously released and this release was increased by TRH and decreased by DA. Both TRH-induced secretion and DA-induced inhibition of prolactin release were dose-dependent with a half maximal effect obtained at 7 x lo-' M for TRH and at lo-' M for DA. It was shown by reverse hemolytic plaque assay that about 55% of the cells were plaque-forming (lysis of red blood cells) and were thus identified as prolactin-secreting cells. This was similar to a previous result obtained by immunofluorescent staining. Heterogeneity among lactotrophs with regard to the quantity of prolactin released was clearly shown by the varying plaque areas in all preparations. In order to make a quantitative analysis of the effect of 178-estradiol on TRH-stimulation and DAergic inhibition in these heterogeneous prolactin cells, they were divided into two groups: large plaques ( 2 3 x lo3 pm') constituted about 35% of all plaque-forming cells, and small plaques ( < 3 x l o 3 pm'), about 65%. Pretreatment with 178-estradiol (lo-' M) either for 10 h or 48 h markedly increased TRH-stimulated prolactin release and decreased the inhibitory effect of DA both in perifusion and reverse hemolytic plaque assay experiments. However, these pretreatments did not change the values of half maximum dose for TRH and DA. TRH transformed about 7% of the small plaques into large plaques and this proportion was increased to 25% after 178-estradiol treatment. On the contrary, DA and its more stable analogue bromocriptine increased the percentage of small plaques by 10% to 15% but this effect was decreased after 178-estradiol treatment. We conclude that: 1) Normal rat pituitary lactotrophs show heterogeneity with respect to their spontaneous release and responsiveness to TRH and DA; 2) pretreatment with 178-estradiol increases the response to TRH and decreases the response to DA without altering the doses at which they have half maximal effect; 3) there is no significant difference between the effect of 17fl-estradiol obtained after 10 h and after 48 h pretreatment.It has long been shown that estrogens play a modulatory role in the control of prolactin (PRL) secretion although its mode of action remains unclear. Pretreatment with 17B-estradiol has been shown to increase the number of thyrotropin-releasing hormone (TRH) binding sites in pituitary homogenates from female rats, whilst concomitantly enhancing the amount of PRL released in response to iv injection of TRH (1, 2). Similarly, in tumoral PRL e l l s in culture, the number of TRH binding sites and TRHinduced PRL...

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“…In a study of ovariectomized rats, both E2 and P4 negatively influenced the activity of neuroendocrine dopaminergic neurons and increased prolactin secretion [19]. E2 has also been shown to decrease the number of dopamine receptors in the anterior pituitary [20,21]. Cloned prolactin-producing GH3 cells also have E2 and P4 receptors [22], and GH3 cell function was shown to be modulated by these steroids.…”

Section: Discussionmentioning

confidence: 99%

Effects of estradiol and progesterone on prolactin transcriptional activity in somatolactotrophic cells

et al. 2012

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THE SEX STEROIDS estradiol (E2) and progesterone (P4) regulate the synthesis and secretion of several pituitary hormones, and play a key role in the regulation of reproductive function. Lactotroph cells, which produce prolactin, are a known target of E2 action. Lactotrophs constitute approximately 15% of the cells of the adenohypophysis; however, this proportion is dependent on age and sex [1]. It has been reported that there is marked hyperplasia of lactotrophs during pregnancy and lactation in humans [2]. Exogenous E2 is known to induce lactotroph hyperplasia [3], and increases prolactin release from rat pituitary cultures by desensitizating lactotrophs to dopamine, a well-known inhibitor of prolactin release [4]. E2 was also reported Effects of estradiol and progesterone on prolactin transcriptional activity in somatolactotrophic cells Tselmeg Mijiddorj, Haruhiko Kanasaki, Indri Purwana, Sukhbaatar Unurjargal, Aki Oride and Kohji Miyazaki Department of Obstetrics and Gynecology, Shimane University School of Medicine, Izumo 693-8501, JapanAbstract. We examined the effects of sex steroids on prolactin promoter activity in rat somatolactotrophic GH3 cells. Both estradiol (E2) and progesterone (P4) were found to inhibit basal prolactin promoter activity, but to potentiate Thyrotropinreleasing hormone (TRH)-induced prolactin promoter activity. P4 had a greater inhibitory effect on basal prolactin promoter activity than E2, and P4 also potentiated TRH-induced prolactin promoter more potently than E2. Combined treatment with E2 and P4 further increased TRH-induced prolactin promoter activity. E2 and P4 also both reduced basal serum response element (SRE) promoter activity, and increased TRH-induced SRE promoter activity. Combination treatment with E2 and P4 reduced basal activity of SRE promoter and increased TRH-induced SRE activity more potently than E2 or P4 alone. In contrast, basal cAMP response element (CRE) promoter activity was not influenced by either E2 or P4, although TRHinduced CRE promoter was potentiated by each of these steroids, and was further increased by E2 and P4 combination treatment. Both E2 and P4 increased TRH-induced extracellular signal-regulated kinase (ERK) phosphorylation; however, intracellular cAMP levels was not influenced by E2 or P4. TRH-induced CRE promoter was inhibited by mitogen-activated protein kinase/ERK kinase (MEK) inhibitor and was increased by overexpression of MEK kinase (MEKK). This study showed that ERK and SRE transcriptional pathways, but not the cAMP/CRE pathway, may be involved in the suppression of basal prolactin promoter activity, whereas both the ERK/SRE and MAP kinase-mediated CRE pathways appear to be involved in the increased transcriptional efficiency of the prolactin promoter induced by TRH stimulation.Key words: Prolactin, Thyrotropin-releasing hormone (TRH), Estradiol, Progesterone, GH3 cells to stimulate lactotroph proliferation and prolactin gene expression in rats [5].E2 modulates gene expression through estrogen receptors (ERs), which belong to the n...

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Modulation of anterior pituitary dopamine receptors by estradiol 17‐β: Dose‐response relationship

Cited by 22 publications

References 18 publications

Cyclosporine Effects on in vitro Responsiveness of Anterior Pituitary Hormone Release to Dopamine and Thyrotropin‐Releasing Hormone in Young Female Rats

Cyclosporine Effects on in vitro Responsiveness of Anterior Pituitary Hormone Release to Dopamine and Thyrotropin‐Releasing Hormone in Young Female Rats

In vitro Effects of 17Beta‐Estradiol on Thyrotropin‐Releasing Hormone‐Induced and Dopamine‐lnhibited Prolactin Release from Adult Male Rat Lactotrophs in Primary Culture

Effects of estradiol and progesterone on prolactin transcriptional activity in somatolactotrophic cells

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