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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<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>
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<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>
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