Progesterone Promotes Rapid Desensitization of α&lt;sub&gt;1&lt;/sub&gt;-Adrenergic Receptor Augmentation of cAMP Formation in Rat Hypothalamic Slices

Petitti, Nicolas; Etgen, Anne M.

doi:10.1159/000126089

Cited by 51 publications

(13 citation statements)

References 32 publications

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“…In contrast, preincubation of rat hypothalamic slices with progesterone (20 nM) for 5 min significantly suppressed norepinephrine-stimulated cAMP formation by Ͼ60%. This effect was estrogen dependent in that progesterone in vitro did not inhibit NE-stimulated cAMP accumulation in slices from ovariectomized rats not pretreated with estradiol (371). In addition, progesterone was found to decrease cAMP levels in quiescent adipocytes or in adipocytes stimulated by isoproterenol (470).…”

Section: B Progesteronementioning

confidence: 91%

Nongenomic Steroid Action: Controversies, Questions, and Answers

Lösel

Falkenstein

Feuring

et al. 2003

Physiological Reviews

503

321

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Lösel, Ralf M., Elisabeth Falkenstein, Martin Feuring, Armin Schultz, Hanns-Christian Tillmann, Karin Rossol-Haseroth, and Martin Wehling. Nongenomic Steroid Action: Controversies, Questions, and Answers. Physiol Rev 83: 965–1016, 2003; 10.1152/physrev.00003.2003.—Steroids may exert their action in living cells by several ways: 1) the well-known genomic pathway, involving hormone binding to cytosolic (classic) receptors and subsequent modulation of gene expression followed by protein synthesis. 2) Alternatively, pathways are operating that do not act on the genome, therefore indicating nongenomic action. Although it is comparatively easy to confirm the nongenomic nature of a particular phenomenon observed, e.g., by using inhibitors of transcription or translation, considerable controversy exists about the identity of receptors that mediate these responses. Many different approaches have been employed to answer this question, including pharmacology, knock-out animals, and numerous biochemical studies. Evidence is presented for and against both the participation of classic receptors, or proteins closely related to them, as well as for the involvement of yet poorly understood, novel membrane steroid receptors. In addition, clinical implications for a wide array of nongenomic steroid actions are outlined.

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Section: B Progesteronementioning

confidence: 91%

Nongenomic Steroid Action: Controversies, Questions, and Answers

Lösel

Falkenstein

Feuring

et al. 2003

Physiological Reviews

503

321

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“…Progesterone may activate membrane receptors coupled to G-proteins [Majewska, 1992;Petitti and Etgen, 1992;Valera et al, 1992;Grazzini et al, 1998]. Progesterone mobilizes calcium from the endoplasmic reticulum and increases the formation of inositol trisphosphate and diacylglycerol via a G-protein insensitive to pertussis toxin in osteoblasts, the bone forming cells, as well as in ovarian granulosa cells .…”

mentioning

confidence: 99%

Membrane signaling and progesterone in female and male osteoblasts. II. Direct involvement of G?q/11 coupled to PLC-?1 and PLC-?3

Mellay

Lieberherr

2000

J. Cell. Biochem.

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We have shown that progesterone (10 pM-10 nM) and progesterone covalently bound to bovine serum albumin (P-CMO BSA; 100 pM-1 microM) rapidly increased (within 5 s) the cytosolic free Ca(2+) concentration and inositol 1,4,5 trisphosphate (InsP(3)) formation in confluent female and male rat osteoblasts via a pertussis toxin-insensitive G-protein. The activation of G-proteins coupled to effectors such as phospholipase C (PLC) is an early event in the signal transduction pathway leading to InsP(3) formation. We used antibodies against the various PLC isoforms to show that only PLC-beta1 and PLC-beta 3 were involved in the Ca(2+) mobilization and InsP(3) formation induced by both progestins in female and male osteoblasts, whereas PLC-beta 2, PLC-gamma 1, and PLC-gamma 2 were not. We also used antibodies against the subunits of heterotrimeric G-proteins to show that the activation of PLC-beta 1 and PLC-beta 3 by both progestins involved the G alpha q/11 subunit, which was insensitive to pertussis toxin, whereas G alpha i, G alpha s, and G beta gamma subunits were not. The membrane effects were independent of the concentration of nuclear progesterone receptor, because the concentration of nuclear progesterone receptors was lower in male than in female osteoblasts. These data suggest that progesterone and P-CMO BSA, which does not enter the cell, directly activate G-protein leading to the very rapid formation of second messengers without involving the nuclear receptor.

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“…Although numerous studies have suggested that P may affect neurotransmission through a nonnuclear action [25,38,39], little is known about the precise molecular mechanisms underlying such interactions. P can interca late into the lipid bilayer of the cell membrane [40], Thus, the modified lipid environment might be the cause of changes in the three-dimensional structure of 5-HTia receptors resulting in a change in the coupling mecha nisms between the receptor and its agonist or between the receptor and G proteins.…”

Section: Effect O F 8-oh-dpat On Lhrh Release From Fetal Hypothalamicmentioning

confidence: 99%

Stimulatory Effects of 5HT<sub>1A</sub> Receptor Agonists on Luteinizing Hormone-Releasing Hormone Release from Cultured Fetal Rat Hypothalamic Cells: Interactions with Progesterone

Héry¹,

Becquet²,

François‐Bellan³

et al. 1995

Neuroendocrinology

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Previous works have suggested an interactive stimulatory effect of progesterone (P) and serotonin (5-HT) on luteinizing hormone release. The purpose of the present study was to determine whether 5-HT via 5-HT_1A receptors interacts with P in the process of luteinizing hormone-releasing hormone (LHRH) release. Using fetal hypothalamic neurons in primary cell cultures the first goal of this study was to determine the effects of 5-HT_1A receptor agonists on LHRH secretion. 8-Hydroxy-2 (di-n-propylamino) tetralin (8-OH-DPAT) or ipsapirone (10^–5M) significantly stimulated LHRH release. Pharmacological studies have allowed to rule out the possible involvement of α₂-or β-adrenore-ceptors, or 5-HT uptake sites, in the stimulatory effect of 8-OH-DPAT on LHRH release, thus demonstrating the specific involvement of 5-HT_1A receptors in the stimulation of LHRH release. The second goal was to test the ability of P to stimulate LHRH release from fetal hypothalamic neurons. P (10^–6M) applied for 30 or 120 min significantly stimulated LHRH secretion. The maintenance of the stimulation of LHRH release by P after a cycloheximide treatment or by an impermeable analog of P, P-3-BSA, has suggested a nonge-nomic effect of P on LHRH release. The effects of a pretreatment of cells by P on 8-OH-DPAT-induced LHRH release were tested. While 10^–7M P alone did not stimulate LHRH release, this concentration of steroid potentiated the LHRH response to 10^–5M 8-OH-DPAT. These findings led to the conclusion that P acting at the level of the plasma membrane potentiates the stimulatory effect of 5-HT_1A receptor agonists on LHRH release.

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Progesterone Promotes Rapid Desensitization of α<sub>1</sub>-Adrenergic Receptor Augmentation of cAMP Formation in Rat Hypothalamic Slices

Cited by 51 publications

References 32 publications

Nongenomic Steroid Action: Controversies, Questions, and Answers

Nongenomic Steroid Action: Controversies, Questions, and Answers

Membrane signaling and progesterone in female and male osteoblasts. II. Direct involvement of G?q/11 coupled to PLC-?1 and PLC-?3

Stimulatory Effects of 5HT<sub>1A</sub> Receptor Agonists on Luteinizing Hormone-Releasing Hormone Release from Cultured Fetal Rat Hypothalamic Cells: Interactions with Progesterone

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