Upregulation of acid-sensing ion channel ASIC1a in spinal dorsal horn neurons contributes to inflammatory pain hypersensitivity
文献类型：期刊论文
| 作者 | Duan B1,2; Wu LJ1; Yu YQ3; Ding Y1; Jing L1,4; Xu L4; Chen J3; Xu TL[*]1,2 |
| 刊名 | JOURNAL OF NEUROSCIENCE
 |
| 出版日期 | 2007 |
| 卷号 | 27期号:41页码:11139-11148 |
| 关键词 | acid-sensing ion channel spinal dorsal horn calcium plasticity inflammation chronic pain sensitization |
| ISSN号 | 0270-6474 |
| 通讯作者 | tlxu@ion.ac.cn |
| 英文摘要 | Development of chronic pain involves alterations in peripheral nociceptors as well as elevated neuronal activity in multiple regions of the CNS. Previous pharmacological and behavioral studies suggest that peripheral acid-sensing ion channels (ASICs) contribute to pain sensation, and the expression of ASIC subunits is elevated in the rat spinal dorsal horn (SDH) in an inflammatory pain model. However, the cellular distribution and the functional consequence of increased ASIC subunit expression in the SDH remain unclear. Here, we identify the Ca2+-permeable, homomeric ASIC1a channels as the predominant ASICs in rat SDH neurons and downregulation of ASIC1a by local rat spinal infusion with specific inhibitors or antisense oligonucleotides markedly attenuated complete Freund's adjuvant (CFA)-induced thermal and mechanical hypersensitivity. Moreover, in vivo electrophysiological recording showed that the elevated ASIC1a activity is required for two forms of central sensitization: C-fiber-induced "wind- up" and CFA-induced hypersensitivity of SDH nociceptive neurons. Together, our results reveal that increased ASIC activity in SDH neurons promotes pain by central sensitization. Specific blockade of Ca2+-permeable ASIC1a channels thus may have antinociceptive effect by reducing or preventing the development of central sensitization induced by inflammation. |
| 收录类别 | SCI |
| 资助信息 | This work was supported by National Natural Science Foundation of China Grants 30500116 and 30621062, National Basic Research Program of China Grant 2006CB500800 |
| 原文出处 | 20072711139.pdf |
| 语种 | 英语 |
| 公开日期 | 2010-08-24 |
| 源URL | [http://159.226.149.42:8088/handle/152453/5905]  |
| 专题 | 昆明动物研究所_学习记忆的分子神经机制 |
| 作者单位 | 1.Institute of Neuroscience and State Key Laboratory of Neuroscience, Chinese Academy of Sciences, Shanghai 200031, Chi 2.School of Life Sciences, University of Science and Technology of China, Hefei 230027, China 3.Institute for Biomedical Sciences of Pain and Functional Brain Disorders, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China 4.Laboratory of Learning and Memory, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China |
| 推荐引用方式 GB/T 7714 | Duan B,Wu LJ,Yu YQ,et al. Upregulation of acid-sensing ion channel ASIC1a in spinal dorsal horn neurons contributes to inflammatory pain hypersensitivity[J]. JOURNAL OF NEUROSCIENCE,2007,27(41):11139-11148. |
| APA | Duan B.,Wu LJ.,Yu YQ.,Ding Y.,Jing L.,...&Xu TL[*].(2007).Upregulation of acid-sensing ion channel ASIC1a in spinal dorsal horn neurons contributes to inflammatory pain hypersensitivity.JOURNAL OF NEUROSCIENCE,27(41),11139-11148. |
| MLA | Duan B,et al."Upregulation of acid-sensing ion channel ASIC1a in spinal dorsal horn neurons contributes to inflammatory pain hypersensitivity".JOURNAL OF NEUROSCIENCE 27.41(2007):11139-11148. |
入库方式： OAI收割
来源：昆明动物研究所
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