Roles of the AMPA receptor subunit GluA1 but not GluA2 in synaptic potentiation and activation of ERK in the anterior cingulate cortex.
Roles of the AMPA receptor subunit GluA1 but not GluA2 in synaptic potentiation and activation of ERK in the anterior cingulate cortex.
复制标题
DOI：
10.1186/1744-8069-5-46
复制
发表时间：
2009-08-10
期刊：
影响因子：
3.3
通讯作者：
Zhuo M
中科院分区：
文献类型：
--
作者：
Toyoda H;Zhao MG;Ulzhöfer B;Wu LJ;Xu H;Seeburg PH;Sprengel R;Kuner R;Zhuo M
包括前扣带回皮质(ACC)在内的皮质区域对疼痛和快乐都很重要。最近利用遗传学和生理学方法的研究表明，对ACC中长时程增强(LTP)的基本机制的研究可能揭示皮层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)受体在LTP的诱导中起关键作用，包括NR2A和NR2B亚基。然而，对ACC LTP表达的细胞和分子机制研究较少。在这里，我们报告了α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic酸(AMPA)受体亚单位GluA1，而不是GluA2，在缺乏GluA1或GluA2基因的遗传操纵小鼠中对ACC中的LTP有贡献。此外，在体内炎性疼痛模型中，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受体亚单位GluA1是ACC LTP表达和炎症诱导的ACC长期可塑性变化的关键机制。
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 α-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.
登录
查看更多内容
影响因子：
64.8
作者：
CRAIR, MC;MALENKA, RC
通讯作者：
MALENKA, RC
影响因子：
5.3
作者：
Ji, RR;Befort, K;Woolf, CJ
通讯作者：
Woolf, CJ
影响因子：
56.9
作者：
Hayashi, Y;Shi, SH;Malinow, R
通讯作者：
Malinow, R
影响因子：
4.7
作者：
Collingridge GL;Olsen RW;Peters J;Spedding M
通讯作者：
Spedding M
影响因子：
5.3
作者：
Phillips, Keith G.;Hardingham, Neil R.;Fox, Kevin
通讯作者：
Fox, Kevin