Activation of Membrane Estrogen Receptors Attenuates NOP-Mediated Tactile Antihypersensitivity in a Rodent Model of Neuropathic Pain.
Identifieur interne : 000684 ( PubMed/Checkpoint ); précédent : 000683; suivant : 000685Activation of Membrane Estrogen Receptors Attenuates NOP-Mediated Tactile Antihypersensitivity in a Rodent Model of Neuropathic Pain.
Auteurs : Danyeal M. Wright [États-Unis] ; Keri M. Small [États-Unis] ; Subodh Nag [États-Unis] ; Sukhbir S. Mokha [États-Unis]Source :
- Brain sciences [ 2076-3425 ] ; 2019.
Abstract
Women manifest a higher prevalence of several chronic pain disorders compared to men. We demonstrated earlier that estrogen rapidly attenuates nociceptin/orphanin FQ (N/OFQ) peptide receptor (NOP)-mediated thermal antinociception through the activation of membrane estrogen receptors (mERs). However, the effect of mER activation on NOP-mediated attenuation of tactile hypersensitivity in a neuropathic model of pain and the underlying mechanisms remain unknown. Following spared nerve injury (SNI), male and ovariectomized (OVX) female rats were intrathecally (i.t.) injected with a selective mER agonist and nociceptin/orphanin FQ (N/OFQ), the endogenous ligand for NOP, and their effects on paw withdrawal thresholds (PWTs) were tested. In addition, spinal cord tissue was used to measure changes in phosphorylated extracellular signal regulated kinase (ERK), protein kinase A (PKA), protein kinase C (PKC), and protein kinase B (Akt) levels. SNI significantly reduced PWTs in males and OVX females, indicating tactile hypersensitivity. N/OFQ restored PWTs, indicating an antihypersensitive effect. Selective mER activation attenuated the effect of N/OFQ in an antagonist-reversible manner. SNI led to a robust increase in the phosphorylation of ERK, PKA, PKC, and Akt. However, mER activation did not further affect it. Thus, we conclude that activation of mERs rapidly abolishes NOP-mediated tactile antihypersensitivity following SNI via an ERK-, PKA-, PKC-, and Akt-independent mechanism.
DOI: 10.3390/brainsci9060147
PubMed: 31234278
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Wright</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208, USA. dheckard@mmc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Small, Keri M" sort="Small, Keri M" uniqKey="Small K" first="Keri M" last="Small">Keri M. Small</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208, USA. kerimcleansmall@gmail.com.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Nag, Subodh" sort="Nag, Subodh" uniqKey="Nag S" first="Subodh" last="Nag">Subodh Nag</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208, USA. snag@mmc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Mokha, Sukhbir S" sort="Mokha, Sukhbir S" uniqKey="Mokha S" first="Sukhbir S" last="Mokha">Sukhbir S. Mokha</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208, USA. smokha@mmc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry, Cancel Biology, 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">Brain sciences</title><idno type="ISSN">2076-3425</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Women manifest a higher prevalence of several chronic pain disorders compared to men. We demonstrated earlier that estrogen rapidly attenuates nociceptin/orphanin FQ (N/OFQ) peptide receptor (NOP)-mediated thermal antinociception through the activation of membrane estrogen receptors (mERs). However, the effect of mER activation on NOP-mediated attenuation of tactile hypersensitivity in a neuropathic model of pain and the underlying mechanisms remain unknown. Following spared nerve injury (SNI), male and ovariectomized (OVX) female rats were intrathecally (i.t.) injected with a selective mER agonist and nociceptin/orphanin FQ (N/OFQ), the endogenous ligand for NOP, and their effects on paw withdrawal thresholds (PWTs) were tested. In addition, spinal cord tissue was used to measure changes in phosphorylated extracellular signal regulated kinase (ERK), protein kinase A (PKA), protein kinase C (PKC), and protein kinase B (Akt) levels. SNI significantly reduced PWTs in males and OVX females, indicating tactile hypersensitivity. N/OFQ restored PWTs, indicating an antihypersensitive effect. Selective mER activation attenuated the effect of N/OFQ in an antagonist-reversible manner. SNI led to a robust increase in the phosphorylation of ERK, PKA, PKC, and Akt. However, mER activation did not further affect it. Thus, we conclude that activation of mERs rapidly abolishes NOP-mediated tactile antihypersensitivity following SNI via an ERK-, PKA-, PKC-, and Akt-independent mechanism.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">31234278</PMID><DateRevised><Year>2020</Year><Month>02</Month><Day>25</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Print">2076-3425</ISSN><JournalIssue CitedMedium="Print"><Volume>9</Volume><Issue>6</Issue><PubDate><Year>2019</Year><Month>Jun</Month><Day>21</Day></PubDate></JournalIssue><Title>Brain sciences</Title><ISOAbbreviation>Brain Sci</ISOAbbreviation></Journal><ArticleTitle>Activation of Membrane Estrogen Receptors Attenuates NOP-Mediated Tactile Antihypersensitivity in a Rodent Model of Neuropathic Pain.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E147</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/brainsci9060147</ELocationID><Abstract><AbstractText>Women manifest a higher prevalence of several chronic pain disorders compared to men. We demonstrated earlier that estrogen rapidly attenuates nociceptin/orphanin FQ (N/OFQ) peptide receptor (NOP)-mediated thermal antinociception through the activation of membrane estrogen receptors (mERs). However, the effect of mER activation on NOP-mediated attenuation of tactile hypersensitivity in a neuropathic model of pain and the underlying mechanisms remain unknown. Following spared nerve injury (SNI), male and ovariectomized (OVX) female rats were intrathecally (i.t.) injected with a selective mER agonist and nociceptin/orphanin FQ (N/OFQ), the endogenous ligand for NOP, and their effects on paw withdrawal thresholds (PWTs) were tested. In addition, spinal cord tissue was used to measure changes in phosphorylated extracellular signal regulated kinase (ERK), protein kinase A (PKA), protein kinase C (PKC), and protein kinase B (Akt) levels. SNI significantly reduced PWTs in males and OVX females, indicating tactile hypersensitivity. N/OFQ restored PWTs, indicating an antihypersensitive effect. Selective mER activation attenuated the effect of N/OFQ in an antagonist-reversible manner. SNI led to a robust increase in the phosphorylation of ERK, PKA, PKC, and Akt. However, mER activation did not further affect it. Thus, we conclude that activation of mERs rapidly abolishes NOP-mediated tactile antihypersensitivity following SNI via an ERK-, PKA-, PKC-, and Akt-independent mechanism.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wright</LastName><ForeName>Danyeal M</ForeName><Initials>DM</Initials><Identifier Source="ORCID">0000-0002-7632-0161</Identifier><AffiliationInfo><Affiliation>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208, USA. dheckard@mmc.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Small</LastName><ForeName>Keri M</ForeName><Initials>KM</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208, USA. kerimcleansmall@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nag</LastName><ForeName>Subodh</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-8834-4278</Identifier><AffiliationInfo><Affiliation>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208, USA. snag@mmc.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mokha</LastName><ForeName>Sukhbir S</ForeName><Initials>SS</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Cancel Biology, Neuroscience and Pharmacology, Meharry Medical College, Nashville, TN 37208, USA. smokha@mmc.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>SC1NS078778</GrantID><Agency>National Institutes of Health</Agency><Country></Country></Grant><Grant><GrantID>R25 GM59994</GrantID><Agency>National Institutes of Health</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>06</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Brain Sci</MedlineTA><NlmUniqueID>101598646</NlmUniqueID><ISSNLinking>2076-3425</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">analgesia</Keyword><Keyword MajorTopicYN="N">neuropathic pain</Keyword><Keyword MajorTopicYN="N">nociceptin/orphanin FQ receptor</Keyword><Keyword MajorTopicYN="N">spared nerve injury</Keyword><Keyword MajorTopicYN="N">spinal cord</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>05</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>06</Month><Day>16</Day></PubMedPubDate><PubMedPubDate 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Wright</name></region><name sortKey="Mokha, Sukhbir S" sort="Mokha, Sukhbir S" uniqKey="Mokha S" first="Sukhbir S" last="Mokha">Sukhbir S. Mokha</name><name sortKey="Nag, Subodh" sort="Nag, Subodh" uniqKey="Nag S" first="Subodh" last="Nag">Subodh Nag</name><name sortKey="Small, Keri M" sort="Small, Keri M" uniqKey="Small K" first="Keri M" last="Small">Keri M. Small</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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