Estrogen in the anterior cingulate cortex contributes to pain-related aversion.
Identifieur interne : 001F98 ( Main/Exploration ); précédent : 001F97; suivant : 001F99Estrogen 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
Affiliations:
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Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></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><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Yang, Yan" sort="Yang, Yan" uniqKey="Yang Y" first="Yan" last="Yang">Yan Yang</name><name sortKey="Zhang, Xiao Meng" sort="Zhang, Xiao Meng" uniqKey="Zhang X" first="Xiao-Meng" last="Zhang">Xiao-Meng Zhang</name><name sortKey="Zhang, Yan" sort="Zhang, Yan" uniqKey="Zhang Y" first="Yan" last="Zhang">Yan Zhang</name><name sortKey="Zhang, Yu Qiu" sort="Zhang, Yu Qiu" uniqKey="Zhang Y" first="Yu-Qiu" last="Zhang">Yu-Qiu Zhang</name><name sortKey="Zhao, Zhi Qi" sort="Zhao, Zhi Qi" uniqKey="Zhao Z" first="Zhi-Qi" last="Zhao">Zhi-Qi Zhao</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Xiao, Xiao" sort="Xiao, Xiao" uniqKey="Xiao X" first="Xiao" last="Xiao">Xiao Xiao</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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