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α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体亚基GluA1而非GluA2在前扣带皮层突触增强和细胞外信号调节激酶（ERK）激活中的作用。

Roles of the AMPA receptor subunit GluA1 but not GluA2 in synaptic potentiation and activation of ERK in the anterior cingulate cortex.

作者信息

Toyoda Hiroki, Zhao Ming-Gao, Ulzhöfer Bettina, Wu Long-Jun, Xu Hui, Seeburg Peter H, Sprengel Rolf, Kuner Rohini, Zhuo Min

机构信息

Department of Physiology, Faculty of Medicine, University of Toronto, University of Toronto Centre for the Study of Pain, 1 King's College Circle, Ontario, Canada.

出版信息

Mol Pain. 2009 Aug 10;5:46. doi: 10.1186/1744-8069-5-46.

DOI:10.1186/1744-8069-5-46
PMID:19664265
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2734546/
Abstract

Cortical areas including the anterior cingulate cortex (ACC) are important for pain and pleasure. Recent studies using genetic and physiological approaches have demonstrated that the investigation of basic mechanism for long-term potentiation (LTP) in the ACC may reveal key cellular and molecular mechanisms for chronic pain in the cortex. Glutamate N-methyl D-aspartate (NMDA) receptors in the ACC are critical for the induction of LTP, including both NR2A and NR2B subunits. However, cellular and molecular mechanisms for the expression of ACC LTP have been less investigated. Here, we report that the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit, GluA1 but not GluA2 contributes to LTP in the ACC using genetic manipulated mice lacking GluA1 or GluA2 gene. Furthermore, GluA1 knockout mice showed decreased extracellular signal-regulated kinase (ERK) phosphorylation in the ACC in inflammatory pain models in vivo. Our results demonstrate that AMPA receptor subunit GluA1 is a key mechanism for the expression of ACC LTP and inflammation-induced long-term plastic changes in the ACC.

摘要

包括前扣带回皮质（ACC）在内的皮质区域对疼痛和愉悦感至关重要。最近使用遗传学和生理学方法进行的研究表明，对ACC中长时程增强（LTP）基本机制的研究可能会揭示皮质慢性疼痛的关键细胞和分子机制。ACC中的谷氨酸N-甲基-D-天冬氨酸（NMDA）受体对LTP的诱导至关重要，包括NR2A和NR2B亚基。然而，对于ACC中LTP表达的细胞和分子机制的研究较少。在此，我们报告使用缺乏GluA1或GluA2基因的基因操纵小鼠，α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体亚基GluA1而非GluA2对ACC中的LTP有贡献。此外，在体内炎症性疼痛模型中，GluA1基因敲除小鼠的ACC中细胞外信号调节激酶（ERK）磷酸化水平降低。我们的结果表明，AMPA受体亚基GluA1是ACC中LTP表达以及ACC中炎症诱导的长期可塑性变化的关键机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/37866fbc711e/1744-8069-5-46-8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/36e62495bc92/1744-8069-5-46-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/afa975c728c2/1744-8069-5-46-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/981de64976a5/1744-8069-5-46-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/3abafcaefe5b/1744-8069-5-46-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/cd4dd751cfe1/1744-8069-5-46-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/edcb55c57003/1744-8069-5-46-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/c62dd742b4b6/1744-8069-5-46-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/37866fbc711e/1744-8069-5-46-8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/36e62495bc92/1744-8069-5-46-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/afa975c728c2/1744-8069-5-46-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/981de64976a5/1744-8069-5-46-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/3abafcaefe5b/1744-8069-5-46-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/cd4dd751cfe1/1744-8069-5-46-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/edcb55c57003/1744-8069-5-46-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/c62dd742b4b6/1744-8069-5-46-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/281c/2734546/37866fbc711e/1744-8069-5-46-8.jpg

相似文献

[1]
Roles of the AMPA receptor subunit GluA1 but not GluA2 in synaptic potentiation and activation of ERK in the anterior cingulate cortex.

Mol Pain. 2009-8-10

[2]
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[3]
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[4]
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[5]
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[6]
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[4]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Activity pattern-dependent long-term potentiation in neocortex and hippocampus of GluA1 (GluR-A) subunit-deficient mice.

J Neurosci. 2009-4-29

[2]
Induction and expression of GluA1 (GluR-A)-independent LTP in the hippocampus.

Eur J Neurosci. 2009-3

[3]
Activation of extracellular signal-regulated kinase in the anterior cingulate cortex contributes to the induction and expression of affective pain.

J Neurosci. 2009-3-11

[4]
Postsynaptic action potentials are required for nitric-oxide-dependent long-term potentiation in CA1 neurons of adult GluR1 knock-out and wild-type mice.

J Neurosci. 2008-12-24

[5]
Enhancement of presynaptic glutamate release and persistent inflammatory pain by increasing neuronal cAMP in the anterior cingulate cortex.

Mol Pain. 2008-9-29

[6]
Cingulate NMDA NR2B receptors contribute to morphine-induced analgesic tolerance.

Mol Brain. 2008-6-17

[7]
Delivery of AMPA receptors to perisynaptic sites precedes the full expression of long-term potentiation.

Proc Natl Acad Sci U S A. 2008-8-12

[8]
A nomenclature for ligand-gated ion channels.

Neuropharmacology. 2009-1

[9]
Activation of Erk in the anterior cingulate cortex during the induction and expression of chronic pain.

Mol Pain. 2008-7-23

[10]
Presynaptic and postsynaptic amplifications of neuropathic pain in the anterior cingulate cortex.

J Neurosci. 2008-7-16

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