Dorsal horn alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor trafficking in inflammatory pain.
Dorsal horn alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor trafficking in inflammatory pain.
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DOI：
10.1097/aln.0b013e3181d3e1ed
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发表时间：
2010-05
期刊：
影响因子：
8.8
通讯作者：
Tao YX
中科院分区：
文献类型：
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作者：
Tao YX
脊髓背角神经元突触N-甲基-d-天冬氨酸受体及其胞内下游信号的激活有助于中枢敏化，这是持续性疼痛中疼痛超敏反应的发展和维持的基础机制。然而，这一事件的分子过程尚未完全了解。最近的研究表明，外周炎症损伤通过N-甲基-d-天冬氨酸受体触发的背角蛋白激酶的激活驱动α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体亚基运输的变化，并提出这种变化可能有助于持续性疼痛的中枢敏感化。本文综述了持续性炎性疼痛条件下背角α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体亚基GluR 1和GluR 2的运输变化，并讨论了这种变化参与炎性疼痛发展和维持的潜在机制。
Activation of synaptic N-methyl-d-aspartic acid receptor and its intracellular downstream signals in dorsal horn neurons of spinal cord contribute to central sensitization, a mechanism that underlies the development and maintenance of pain hypersensitivity in persistent pain. However, the molecular process of this event is not completely understood. Recently, new studies suggest that peripheral inflammatory insults drive changes in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit trafficking via N-methyl-d-aspartic acid receptor-triggered activation of protein kinases in dorsal horn and raise the possibility that such changes might contribute to central sensitization in persistent pain. This review presents current evidence regarding the changes that occur in the trafficking of dorsal horn α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunits GluR1 and GluR2 under persistent inflammatory pain conditions and discusses potential mechanisms by which such changes participate in the development and maintenance of inflammatory pain.