Membrane estradiol signaling in the brain

Micevych, Paul; Dominguez, Reymundo

doi:10.1016/j.yfrne.2009.04.011

Cited by 177Estrogen and related hormone effectsNeuroscience and Neuropharmacology ResearchReceptor Mechanisms and Signaling

Membrane estradiol signaling in the brain

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Micevych, Paul, Dominguez, Reymundo·2009·Frontiers in Neuroendocrinology

DOI 10.1016/j.yfrne.2009.04.011PMC PMC2720427

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Abstract

While the physiology of membrane-initiated estradiol signaling in the nervous system has remained elusive, a great deal of progress has been made toward understanding the activation of cell signaling. Membrane-initiated estradiol signaling activates G proteins and their downstream cascades, but the identity of membrane receptors and the proximal signaling mechanism(s) have been more difficult to elucidate. Mounting evidence suggests that classical intracellular estrogen receptor-alpha (ERalpha) and ERbeta are trafficked to the membrane to mediate estradiol cell signaling. Moreover, an interaction of membrane ERalpha and ERbeta with metabotropic glutamate receptors has been identified that explains the pleomorphic actions of membrane-initiated estradiol signaling. This review focuses on the mechanism of actions initiated by membrane estradiol receptors and discusses the role of scaffold proteins and signaling cascades involved in the regulation of nociception, sexual receptivity and the synthesis of neuroprogesterone, an important component in the central nervous system signaling.

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These hypothalamic circuits express various ERs and use nuclear and membrane-initiated estrogen signaling.
“These hypothalamic circuits collectively express the range of ER and employ both nuclear-initiated estrogen signaling (through estrogen response element (ERE)-dependent and ERE-independent pathways) and membrane-initiated estrogen signaling (through palmitoylated nuclear ER (α/β) and E2-responsive GPCR)34.”
From Emerging insights into hypothalamic‐pituitary‐gonadal axis regulation and interaction with stress signalling (2018) · cites this paper as [34]
The Introduction describes ERE-dependent and ERE-independent nuclear signaling, while Extranuclear ERα and ERβ Expression and Physiology of Membrane ERs describe membrane signaling in hypothalamic-related circuits. The Summary supports palmitoylated ERα/ERβ at membranes, but Novel ERs treats the E2-responsive GPCR candidates as uncertain rather than establishing that these circuits employ them. Page numbers are unavailable in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measured
After ligand activation, ER leaves chaperones, dimerizes, and binds coactivators or corepressors to start or stop transcription.
“After ligand-dependent receptor activation, ER disassociates from molecular chaperones, dimerizes, and binds to coactivators or corepressors to initiate or suppress transcription34.”
From Emerging insights into hypothalamic‐pituitary‐gonadal axis regulation and interaction with stress signalling (2018) · cites this paper as [34]
The Introduction says that estradiol-bound intracellular ERs dimerize and recruit transcriptional machinery and cofactors to regulate gene expression. It does not say that ERs dissociate from molecular chaperones or specifically bind coactivators or corepressors to initiate or suppress transcription. No page number is available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Nuclear ERα/ERβ signaling mainly controls gene expression by binding DNA at EREs.
“Nuclear-initiated ERα and ERβ signaling controls gene expression primarily through direct binding to DNA via an ERE.”
From Emerging insights into hypothalamic‐pituitary‐gonadal axis regulation and interaction with stress signalling (2018) · cites this paper as [34]
Experimental — accuracy not yet measured
Gonadal steroids can affect cell physiology over the long term by acting as transcription factors to regulate gene expression or rapidly through non-genomic second messenger cascades.
“can affect cell physiology over the long term by acting as transcription factors to regulate gene expression (Heldring et al., 2007) or rapidly through non-genomic second messenger cascades (Micevych and Dominguez, 2009)”
From Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex? (2017) · cites this paper as Micevych and Dominguez, 2009

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Research works printed but not linked: 3

[39]Dewing P Boulware MI Sinchak K Christensen A Mermelstein PG Micevych P Membrane estrogen receptor-alpha interactions with metabotropic glutamate receptor 1a modulate female sexual receptivity in rats J Neurosci 27 2007 9294 9300 17728443 PMC2904398
[86]Kuo J Hariri OR Bondar G Ogi J Micevych PE Membrane estradiol receptors interact with metabotropic glutamate receptors to mobilize intracellular calcium in hypothalamic astrocytes Endocrinology 2008 submitted PMC2654734 18948402
[184]Sinchak K Micevych PE Progesterone blockade of estrogen activation of mu-opioid receptors regulates reproductive behavior J Neurosci 21 2001 5723 5729 11466444 PMC6762652

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Self-citation

Authors: Micevych, P., & Dominguez, R.
Affiliations: University of California, Los Angeles (US)
Corresponding author: Micevych, Paul
ORCID: Micevych, Paul
Dominguez, Reymundo
Venue: Frontiers in Neuroendocrinology
Publisher: Elsevier BV
Published: 2009-08
Volume: 30
Issue: 3
Pages: 315-327
ISSN: 0091-3022 (ISSN-L)
DOI: 10.1016/j.yfrne.2009.04.011
PMC: PMC2720427
OpenAlex: W1980509664
Cited by: 177
References: 231
Citations by year: 2026: 4 · 2025: 1 · 2024: 6 · 2023: 9 · 2022: 3 · 2021: 5 · 2020: 7 · 2019: 7 · 2018: 8 · 2017: 9 · 2016: 9 · 2015: 21 · 2014: 11 · 2013: 20 · 2012: 16
FWCI: 1.80
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Frontiers in Neuroendocrinology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
eCite Digital Repository (University of Tasmania) (submittedVersion)
Figshare (submittedVersion, cc-by)
Funders: National Institute on Aging (AG 14751, P01AG014751)
National Institute on Drug Abuse (DA013185, R01DA013185)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD 042635, R01HD042635, T32HD007228)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords: membrane estrogen receptor, estrogen receptor alpha, estrogen receptor beta, metabotropic glutamate receptors, G protein signaling, scaffold proteins, nociception, sexual receptivity, brain
MeSH terms: Animals, Brain, Cell Membrane, Estradiol, Humans, Models, Biological, Receptors, Estrogen, Signal Transduction

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Membrane estradiol signaling in the brain

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