G protein-coupled estrogen receptor is required for the neuritogenic mechanism of 17β-estradiol in developing hippocampal neurons

Ruiz-Palmero, Isabel; Hernando, María; Garcia-Segura, Luis Miguel; Arévalo, María Ángeles

doi:10.1016/j.mce.2013.03.018

Cited by 67 publications

(55 citation statements)

References 61 publications

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“…The specificities of p-ERK 1/2 and GPER antibodies were reported in previous studies (cell signaling data sheet [35]). Additional assays were performed in order to test their specificity in our material: (a) the primary antibody was omitted or replaced with an equivalent concentration of normal serum (negative controls); (b) the secondary antibody was omitted.…”

Section: Methodsmentioning

confidence: 95%

NADPH-Diaphorase Colocalizes with GPER and Is Modulated by the GPER Agonist G1 in the Supraoptic and Paraventricular Nuclei of Ovariectomized Female Rats

Grassi

Lagunas²,

Pinos³

et al. 2016

Neuroendocrinology

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Nitric oxide is produced in the brain by the neuronal nitric oxide synthase (nNOS) and carries out a wide range of functions by acting as a neurotransmitter-like molecule. Gonadal hormones are involved in the regulation of the brain nitrergic system. We have previously demonstrated that estradiol, via classical estrogen receptors (ERs), regulates NOS activity in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus, acting through both ERα and ERβ. Magnocellular and parvocellular neurons in the SON and PVN also express the G protein-coupled ER (GPER). In this study, we have assessed whether GPER is also involved in the regulation of nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase in the SON and PVN. Adult female ovariectomized rats were treated with G1, a selective GPER agonist, or with G1 in combination with G15, a selective GPER antagonist. G1 treatment decreased NADPH-diaphorase expression in the SON and in all PVN subnuclei. The treatment with G1 + G15 effectively rescued the G1-dependent decrease in NADPH-diaphorase expression in both brain regions. In addition, the activation of extracellular signal-regulated kinase (ERK) 1/2, one of the kinases involved in the GPER-dependent intracellular signaling pathway and in NOS phosphorylation, was assessed in the same brain nuclei. Treatment with G1 significantly decreased the number of p-ERK 1/2-positive cells in the SON and PVN, while the treatment with G1 + G15 significantly recovered its number to control values. These findings suggest that the activation of GPER in the SON and PVN inhibits the phosphorylation of ERK 1/2, which induces a decrease in NADPH-diaphorase expression.

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Section: Methodsmentioning

confidence: 95%

NADPH-Diaphorase Colocalizes with GPER and Is Modulated by the GPER Agonist G1 in the Supraoptic and Paraventricular Nuclei of Ovariectomized Female Rats

Grassi

Lagunas²,

Pinos³

et al. 2016

Neuroendocrinology

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“…Moreover, in endometrial cancer cells that lack ERα, tamoxifen promotes cell migration via activation of GPER1 (Tsai et al, 2013). ICI 182,780 is also reported to have GPER1 agonist activity in neurons as application of ICI 182,780 to hippocampal neurons increased neurogenin 3 expression and neuritogenesis, which mirrored the effects of G1 and E2 (Ruiz-Palmero et al, 2013;RuizPalmero et al, 2011). Moreover the effects of ICI 182,780 were blocked by G15 and following knockdown of GPER1 (Ruiz-Palmero et al, 2013).…”

Section: The Pharmacology Of Gper1mentioning

confidence: 93%

“…ICI 182,780 is also reported to have GPER1 agonist activity in neurons as application of ICI 182,780 to hippocampal neurons increased neurogenin 3 expression and neuritogenesis, which mirrored the effects of G1 and E2 (Ruiz-Palmero et al, 2013;RuizPalmero et al, 2011). Moreover the effects of ICI 182,780 were blocked by G15 and following knockdown of GPER1 (Ruiz-Palmero et al, 2013). Recent studies indicate that the "selective" ERα agonist, propylpyrazole triol (PPT), also has agonist actions at GPER1 (Petrie et al, 2013), which further complicates interpretation of data using this compound.…”

Section: The Pharmacology Of Gper1mentioning

confidence: 93%

Emerging roles for the novel estrogen-sensing receptor GPER1 in the CNS

2017

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Keywords: G protein coupled estrogen receptor, hippocampal synaptic function; receptor trafficking; learning and memory; neuroprotection; synaptic plasticity. Estrogens play a key role in regulating reproductive and neuroendocrine function by activating classical nuclear steroid receptors that act as ligand gated transcription factors.However evidence is growing that estrogens also promote rapid non-genomic responses via activation of membrane-associated estrogen receptors. The G protein-coupled estrogen receptor (GPER1; also known as GPR30) has been identified as one of the main estrogensensitive receptors responsible for the rapid non-genomic actions of estrogen. In recent years, our understanding of the CNS actions of GPER1s has significantly increased following the development of selective pharmacological tools and via the use of transgenic technologies to knockout GPER1 in mice. Here we review recent advances that have been made to uncover the role of GPER1s in the CNS.Introduction.

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“…The role of GPER1 in mediating 17b-estradiol rapid signaling has received little attention, but G1 has been shown to induce a rapid increase in Akt phosphorylation in hippocampal neurons (Ruiz-Palmero et al, 2013). Further, in cancer cells, estrogen rapidly increases GPER1 coimmunoprecipitation with ERa (Vivacqua et al, 2009), suggesting that interaction between those receptors could mediate rapid estrogen effects.…”

Section: Signaling Pathways Activated By Estrogenic Agonistsmentioning

confidence: 99%

Neuroprotection in Parkinsonian-treated mice via estrogen receptor α activation requires G protein-coupled estrogen receptor 1

2015

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G protein-coupled estrogen receptor is required for the neuritogenic mechanism of 17β-estradiol in developing hippocampal neurons

Cited by 67 publications

References 61 publications

NADPH-Diaphorase Colocalizes with GPER and Is Modulated by the GPER Agonist G1 in the Supraoptic and Paraventricular Nuclei of Ovariectomized Female Rats

NADPH-Diaphorase Colocalizes with GPER and Is Modulated by the GPER Agonist G1 in the Supraoptic and Paraventricular Nuclei of Ovariectomized Female Rats

Emerging roles for the novel estrogen-sensing receptor GPER1 in the CNS

Neuroprotection in Parkinsonian-treated mice via estrogen receptor α activation requires G protein-coupled estrogen receptor 1

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