Activation of membrane estrogen receptors attenuates opioid receptor-like1 receptor-mediated antinociception via an ERK-dependent non-genomic mechanism.
Identifieur interne : 002061 ( Main/Curation ); précédent : 002060; suivant : 002062Activation of membrane estrogen receptors attenuates opioid receptor-like1 receptor-mediated antinociception via an ERK-dependent non-genomic mechanism.
Auteurs : K M Small [États-Unis] ; S. Nag [États-Unis] ; S S Mokha [États-Unis]Source :
- Neuroscience [ 1873-7544 ] ; 2013.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Extracellular Signal-Regulated MAP Kinases, Receptors, Estrogen, Receptors, Opioid.
- metabolism : Cell Membrane, Pain.
- Animals, Blotting, Western, Female, Male, Ovariectomy, Rats, Rats, Sprague-Dawley.
Abstract
To our knowledge, the present data are the first to demonstrate that activation of membrane estrogen receptors (mERs) abolishes opioid receptor-like 1 (ORL1) receptor-mediated analgesia via extracellular signal-regulated kinase (ERK)-dependent non-genomic mechanisms. Estrogen was shown previously to both attenuate ORL1-mediated antinociception and down-regulate the ORL1 gene expression. The present study investigated whether non-genomic mechanisms contribute to estrogen-induced attenuation of ORL1-mediated antinociception by the mERs GPR30, Gq-coupled mER, ERα, and ERβ. E2BSA [β-estradiol-6-(O-carboxymethyl)oxime: bovine serum albumin] (0.5mM), a membrane impermeant analog of estradiol, injected intrathecally immediately prior to orphanin FQ (OFQ;10 nmol), the endogenous ligand for the ORL1 receptor, abolished OFQ's antinociceptive effect in both male and ovariectomized (OVX) female rats, assessed using the heat-induced tail-flick assay. This effect was not altered by protein synthesis inhibitor, anisomycin (125 μg), given intrathecally 15 min prior to E2BSA and OFQ. Intrathecal application of selective receptor agonists permitted the relative contributions of various estrogen receptors in mediating this blockade of the antinociceptive response of OFQ. Activation of GPR30, Gq-mER, ERα, but not ERβ abolished ORL1-mediated antinociception in males and OVX females. E2BSA produced a parallel and significant increase in the phosphorylation of ERK 2 only in OVX females, and pre-treatment with MEK/ERK 1/2 inhibitor, U0126 (10 μg), blocked the mER-mediated abolition of ORL1-mediated antinociception in OVX females. Taken together, the data are consistent with the interpretations that mER activation attenuates ORL1-mediated antinociception through a non-genomic, ERK 2-dependent mechanism in females.
DOI: 10.1016/j.neuroscience.2013.10.034
PubMed: 24452062
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Electronic address: smokha@mmc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author></analytic><series><title level="j">Neuroscience</title><idno type="eISSN">1873-7544</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Blotting, Western</term><term>Cell Membrane (metabolism)</term><term>Extracellular Signal-Regulated MAP Kinases (metabolism)</term><term>Female</term><term>Male</term><term>Ovariectomy</term><term>Pain (metabolism)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Receptors, Estrogen (metabolism)</term><term>Receptors, Opioid (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Douleur (métabolisme)</term><term>Extracellular Signal-Regulated MAP Kinases (métabolisme)</term><term>Femelle</term><term>Membrane cellulaire (métabolisme)</term><term>Mâle</term><term>Ovariectomie</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Récepteurs aux opioïdes (métabolisme)</term><term>Récepteurs des oestrogènes (métabolisme)</term><term>Technique de Western</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Extracellular Signal-Regulated MAP Kinases</term><term>Receptors, Estrogen</term><term>Receptors, Opioid</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cell Membrane</term><term>Pain</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Douleur</term><term>Extracellular Signal-Regulated MAP Kinases</term><term>Membrane cellulaire</term><term>Récepteurs aux opioïdes</term><term>Récepteurs des oestrogènes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Blotting, Western</term><term>Female</term><term>Male</term><term>Ovariectomy</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Mâle</term><term>Ovariectomie</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Technique de Western</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To our knowledge, the present data are the first to demonstrate that activation of membrane estrogen receptors (mERs) abolishes opioid receptor-like 1 (ORL1) receptor-mediated analgesia via extracellular signal-regulated kinase (ERK)-dependent non-genomic mechanisms. Estrogen was shown previously to both attenuate ORL1-mediated antinociception and down-regulate the ORL1 gene expression. The present study investigated whether non-genomic mechanisms contribute to estrogen-induced attenuation of ORL1-mediated antinociception by the mERs GPR30, Gq-coupled mER, ERα, and ERβ. E2BSA [β-estradiol-6-(O-carboxymethyl)oxime: bovine serum albumin] (0.5mM), a membrane impermeant analog of estradiol, injected intrathecally immediately prior to orphanin FQ (OFQ;10 nmol), the endogenous ligand for the ORL1 receptor, abolished OFQ's antinociceptive effect in both male and ovariectomized (OVX) female rats, assessed using the heat-induced tail-flick assay. This effect was not altered by protein synthesis inhibitor, anisomycin (125 μg), given intrathecally 15 min prior to E2BSA and OFQ. Intrathecal application of selective receptor agonists permitted the relative contributions of various estrogen receptors in mediating this blockade of the antinociceptive response of OFQ. Activation of GPR30, Gq-mER, ERα, but not ERβ abolished ORL1-mediated antinociception in males and OVX females. E2BSA produced a parallel and significant increase in the phosphorylation of ERK 2 only in OVX females, and pre-treatment with MEK/ERK 1/2 inhibitor, U0126 (10 μg), blocked the mER-mediated abolition of ORL1-mediated antinociception in OVX females. Taken together, the data are consistent with the interpretations that mER activation attenuates ORL1-mediated antinociception through a non-genomic, ERK 2-dependent mechanism in females.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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