Estrogen in the anterior cingulate cortex contributes to pain-related aversion.
Identifieur interne : 001D67 ( PubMed/Curation ); précédent : 001D66; suivant : 001D68Estrogen in the anterior cingulate cortex contributes to pain-related aversion.
Auteurs : Xiao Xiao [République populaire de Chine] ; Yan Yang ; Yan Zhang ; Xiao-Meng Zhang ; Zhi-Qi Zhao ; Yu-Qiu ZhangSource :
- Cerebral cortex (New York, N.Y. : 1991) [ 1460-2199 ] ; 2013.
Descripteurs français
- KwdFr :
- Affect (physiologie), Animaux, Douleur (physiopathologie), Femelle, Gyrus du cingulum (physiopathologie), Mâle, Oestradiol (physiologie), Ovariectomie, Plasticité neuronale, Rat Sprague-Dawley, Rats, Récepteurs des oestrogènes (physiologie), Récepteurs du N-méthyl-D-aspartate (physiologie), Transmission synaptique.
- MESH :
- physiologie : Affect, Oestradiol, Récepteurs des oestrogènes, Récepteurs du N-méthyl-D-aspartate.
- physiopathologie : Douleur, Gyrus du cingulum.
- Animaux, Femelle, Mâle, Ovariectomie, Plasticité neuronale, Rat Sprague-Dawley, Rats, Transmission synaptique.
English descriptors
- KwdEn :
- Affect (physiology), Animals, Conditioning, Psychological (physiology), Estradiol (physiology), Female, Gyrus Cinguli (physiopathology), Male, Neuronal Plasticity, Ovariectomy, Pain (physiopathology), Rats, Rats, Sprague-Dawley, Receptors, Estrogen (physiology), Receptors, N-Methyl-D-Aspartate (physiology), Synaptic Transmission.
- MESH :
- chemical , physiology : Estradiol, Receptors, Estrogen, Receptors, N-Methyl-D-Aspartate.
- physiology : Affect, Conditioning, Psychological.
- physiopathology : Gyrus Cinguli, Pain.
- Animals, Female, Male, Neuronal Plasticity, Ovariectomy, Rats, Rats, Sprague-Dawley, Synaptic Transmission.
Abstract
The rostral anterior cingulate cortex (rACC) is a key structure of pain affect. Whether and how estrogen in the rACC regulates pain-related negative emotion remains unclear. Behaviorally, using formalin-induced conditioned place aversion (F-CPA) in rats, which is believed to reflect the pain-related negative emotion, we found that estrogen receptor (ER) inhibitor ICI 182, 780 (ICI, 7α,17β-[9-[(4,4,5,5,5-Pentafluoropentyl)sulfinyl]nonyl]estra-1,3,5(10)-triene-3,17-diol) or inhibitor of aromatase androstatrienedione into the rACC completely blocked F-CPA in either sex. An analogous effect was also observed in ovariectomy rats. Furthermore, exogenous estrogen in the absence of a formalin noxious stimulus was sufficient to elicit CPA (E-CPA) in both sexes by activating the membrane estrogen receptors (mERs) and N-methyl-D-aspartic acid (NMDA) receptors (NMDARs). Electrophysiologically, we demonstrated that estrogen acutely enhanced the glutamatergic excitatory postsynaptic currents (EPSCs) in rACC slices by increasing the ratio of NMDA-EPSCs to α-amino-3-(5-methyl-3-oxo-1,2- oxazol-4-yl) propanoic acid -EPSCs and presynaptic glutamate release. Interestingly, a brief exposure to estrogen elicited a persistent enhancement of NMDA-EPSCs, and this NMDA-long-term potentiation required the activation of the mERs, protein kinase A and NMDAR subunit NR2B. Finally, estrogen induced rapid dendritic spine formation in cultured rACC neurons. These results suggest that estrogen in the rACC, as a neuromodulator, drives affective pain via facilitating NMDA receptor-mediated synaptic transmission.
DOI: 10.1093/cercor/bhs201
PubMed: 22784608
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cortex contributes to pain-related aversion.</title><author><name sortKey="Xiao, Xiao" sort="Xiao, Xiao" uniqKey="Xiao X" first="Xiao" last="Xiao">Xiao Xiao</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Neurobiology, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Neurobiology, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032</wicri:regionArea></affiliation></author><author><name sortKey="Yang, Yan" sort="Yang, Yan" uniqKey="Yang Y" first="Yan" last="Yang">Yan Yang</name></author><author><name sortKey="Zhang, Yan" sort="Zhang, Yan" uniqKey="Zhang Y" first="Yan" last="Zhang">Yan Zhang</name></author><author><name sortKey="Zhang, Xiao Meng" sort="Zhang, Xiao Meng" uniqKey="Zhang X" first="Xiao-Meng" last="Zhang">Xiao-Meng Zhang</name></author><author><name sortKey="Zhao, Zhi Qi" sort="Zhao, Zhi Qi" uniqKey="Zhao Z" first="Zhi-Qi" last="Zhao">Zhi-Qi Zhao</name></author><author><name sortKey="Zhang, Yu Qiu" sort="Zhang, Yu Qiu" uniqKey="Zhang Y" first="Yu-Qiu" last="Zhang">Yu-Qiu Zhang</name></author></analytic><series><title level="j">Cerebral cortex (New York, N.Y. : 1991)</title><idno type="eISSN">1460-2199</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Affect (physiology)</term><term>Animals</term><term>Conditioning, Psychological (physiology)</term><term>Estradiol (physiology)</term><term>Female</term><term>Gyrus Cinguli (physiopathology)</term><term>Male</term><term>Neuronal Plasticity</term><term>Ovariectomy</term><term>Pain (physiopathology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Receptors, Estrogen (physiology)</term><term>Receptors, N-Methyl-D-Aspartate (physiology)</term><term>Synaptic Transmission</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Affect (physiologie)</term><term>Animaux</term><term>Douleur (physiopathologie)</term><term>Femelle</term><term>Gyrus du cingulum (physiopathologie)</term><term>Mâle</term><term>Oestradiol (physiologie)</term><term>Ovariectomie</term><term>Plasticité neuronale</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Récepteurs des oestrogènes (physiologie)</term><term>Récepteurs du N-méthyl-D-aspartate (physiologie)</term><term>Transmission synaptique</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Estradiol</term><term>Receptors, Estrogen</term><term>Receptors, N-Methyl-D-Aspartate</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Affect</term><term>Oestradiol</term><term>Récepteurs des oestrogènes</term><term>Récepteurs du N-méthyl-D-aspartate</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Affect</term><term>Conditioning, Psychological</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Douleur</term><term>Gyrus du cingulum</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Gyrus Cinguli</term><term>Pain</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Male</term><term>Neuronal Plasticity</term><term>Ovariectomy</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Mâle</term><term>Ovariectomie</term><term>Plasticité neuronale</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Transmission synaptique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The rostral anterior cingulate cortex (rACC) is a key structure of pain affect. Whether and how estrogen in the rACC regulates pain-related negative emotion remains unclear. Behaviorally, using formalin-induced conditioned place aversion (F-CPA) in rats, which is believed to reflect the pain-related negative emotion, we found that estrogen receptor (ER) inhibitor ICI 182, 780 (ICI, 7α,17β-[9-[(4,4,5,5,5-Pentafluoropentyl)sulfinyl]nonyl]estra-1,3,5(10)-triene-3,17-diol) or inhibitor of aromatase androstatrienedione into the rACC completely blocked F-CPA in either sex. An analogous effect was also observed in ovariectomy rats. Furthermore, exogenous estrogen in the absence of a formalin noxious stimulus was sufficient to elicit CPA (E-CPA) in both sexes by activating the membrane estrogen receptors (mERs) and N-methyl-D-aspartic acid (NMDA) receptors (NMDARs). Electrophysiologically, we demonstrated that estrogen acutely enhanced the glutamatergic excitatory postsynaptic currents (EPSCs) in rACC slices by increasing the ratio of NMDA-EPSCs to α-amino-3-(5-methyl-3-oxo-1,2- oxazol-4-yl) propanoic acid -EPSCs and presynaptic glutamate release. Interestingly, a brief exposure to estrogen elicited a persistent enhancement of NMDA-EPSCs, and this NMDA-long-term potentiation required the activation of the mERs, protein kinase A and NMDAR subunit NR2B. Finally, estrogen induced rapid dendritic spine formation in cultured rACC neurons. These results suggest that estrogen in the rACC, as a neuromodulator, drives affective pain via facilitating NMDA receptor-mediated synaptic transmission. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22784608</PMID><DateCompleted><Year>2014</Year><Month>02</Month><Day>10</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2199</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>9</Issue><PubDate><Year>2013</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Cerebral cortex (New York, N.Y. : 1991)</Title><ISOAbbreviation>Cereb. Cortex</ISOAbbreviation></Journal><ArticleTitle>Estrogen in the anterior cingulate cortex contributes to pain-related aversion.</ArticleTitle><Pagination><MedlinePgn>2190-203</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/cercor/bhs201</ELocationID><Abstract><AbstractText>The rostral anterior cingulate cortex (rACC) is a key structure of pain affect. Whether and how estrogen in the rACC regulates pain-related negative emotion remains unclear. Behaviorally, using formalin-induced conditioned place aversion (F-CPA) in rats, which is believed to reflect the pain-related negative emotion, we found that estrogen receptor (ER) inhibitor ICI 182, 780 (ICI, 7α,17β-[9-[(4,4,5,5,5-Pentafluoropentyl)sulfinyl]nonyl]estra-1,3,5(10)-triene-3,17-diol) or inhibitor of aromatase androstatrienedione into the rACC completely blocked F-CPA in either sex. An analogous effect was also observed in ovariectomy rats. Furthermore, exogenous estrogen in the absence of a formalin noxious stimulus was sufficient to elicit CPA (E-CPA) in both sexes by activating the membrane estrogen receptors (mERs) and N-methyl-D-aspartic acid (NMDA) receptors (NMDARs). Electrophysiologically, we demonstrated that estrogen acutely enhanced the glutamatergic excitatory postsynaptic currents (EPSCs) in rACC slices by increasing the ratio of NMDA-EPSCs to α-amino-3-(5-methyl-3-oxo-1,2- oxazol-4-yl) propanoic acid -EPSCs and presynaptic glutamate release. Interestingly, a brief exposure to estrogen elicited a persistent enhancement of NMDA-EPSCs, and this NMDA-long-term potentiation required the activation of the mERs, protein kinase A and NMDAR subunit NR2B. Finally, estrogen induced rapid dendritic spine formation in cultured rACC neurons. These results suggest that estrogen in the rACC, as a neuromodulator, drives affective pain via facilitating NMDA receptor-mediated synaptic transmission. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xiao</LastName><ForeName>Xiao</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Institute of Neurobiology, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Yan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xiao-Meng</ForeName><Initials>XM</Initials></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Zhi-Qi</ForeName><Initials>ZQ</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yu-Qiu</ForeName><Initials>YQ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>07</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cereb Cortex</MedlineTA><NlmUniqueID>9110718</NlmUniqueID><ISSNLinking>1047-3211</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011960">Receptors, Estrogen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016194">Receptors, N-Methyl-D-Aspartate</NameOfSubstance></Chemical><Chemical><RegistryNumber>4TI98Z838E</RegistryNumber><NameOfSubstance UI="D004958">Estradiol</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000339" MajorTopicYN="N">Affect</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003213" MajorTopicYN="N">Conditioning, Psychological</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004958" MajorTopicYN="N">Estradiol</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006179" MajorTopicYN="N">Gyrus Cinguli</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009473" MajorTopicYN="N">Neuronal Plasticity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010052" MajorTopicYN="N">Ovariectomy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010146" MajorTopicYN="N">Pain</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011960" MajorTopicYN="N">Receptors, Estrogen</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016194" MajorTopicYN="N">Receptors, N-Methyl-D-Aspartate</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009435" MajorTopicYN="N">Synaptic Transmission</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">anterior cingulate cortex</Keyword><Keyword MajorTopicYN="N">estrogen and estrogen receptors</Keyword><Keyword MajorTopicYN="N">formalin-induced conditioned place aversion</Keyword><Keyword MajorTopicYN="N">long-term potentiation</Keyword><Keyword MajorTopicYN="N">pain-related aversion</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>7</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>7</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>2</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22784608</ArticleId><ArticleId IdType="pii">bhs201</ArticleId><ArticleId IdType="doi">10.1093/cercor/bhs201</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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