beta-arrestin-2 regulates NMDA receptor function in spinal lamina II neurons and duration of persistent pain
DC Field | Value | Language |
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dc.contributor.author | Chen, Gang | - |
dc.contributor.author | Xie, Rou-Gang | - |
dc.contributor.author | Gao, Yong-Jing | - |
dc.contributor.author | Xu, Zhen-Zhong | - |
dc.contributor.author | Zhao, Lin-Xia | - |
dc.contributor.author | Bang, Sangsu | - |
dc.contributor.author | Berta, Temugin | - |
dc.contributor.author | Park, Chul-Kyu | - |
dc.contributor.author | Lay, Mark | - |
dc.contributor.author | Chen, Wei | - |
dc.contributor.author | Ji, Ru-Rong | - |
dc.date.available | 2020-02-28T01:42:14Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2016-08 | - |
dc.identifier.issn | 2041-1723 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/8071 | - |
dc.description.abstract | Mechanisms of acute pain transition to chronic pain are not fully understood. Here we demonstrate an active role of beta-arrestin 2 (Arrb2) in regulating spinal cord NMDA receptor (NMDAR) function and the duration of pain. Intrathecal injection of the mu-opioid receptor agonist [D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin produces paradoxical behavioural responses: early-phase analgesia and late-phase mechanical allodynia which requires NMDAR; both phases are prolonged in Arrb2 knockout (KO) mice. Spinal administration of NMDA induces GluN2B-dependent mechanical allodynia, which is prolonged in Arrb2-KO mice and conditional KO mice lacking Arrb2 in presynaptic terminals expressing Nav1.8. Loss of Arrb2 also results in prolongation of inflammatory pain and neuropathic pain and enhancement of GluN2B-mediated NMDA currents in spinal lamina IIo not lamina I neurons. Finally, spinal over-expression of Arrb2 reverses chronic neuropathic pain after nerve injury. Thus, spinal Arrb2 may serve as an intracellular gate for acute to chronic pain transition via desensitization of NMDAR. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.relation.isPartOf | NATURE COMMUNICATIONS | - |
dc.subject | PRIMARY SENSORY NEURONS | - |
dc.subject | NEUROPATHIC PAIN | - |
dc.subject | INFLAMMATORY PAIN | - |
dc.subject | DORSAL-HORN | - |
dc.subject | PERIPHERAL NEUROPATHY | - |
dc.subject | CENTRAL SENSITIZATION | - |
dc.subject | MECHANICAL ALLODYNIA | - |
dc.subject | NOCICEPTIVE NEURONS | - |
dc.subject | SYNAPTIC PLASTICITY | - |
dc.subject | MORPHINE-TOLERANCE | - |
dc.title | beta-arrestin-2 regulates NMDA receptor function in spinal lamina II neurons and duration of persistent pain | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000381774900001 | - |
dc.identifier.doi | 10.1038/ncomms12531 | - |
dc.identifier.bibliographicCitation | NATURE COMMUNICATIONS, v.7 | - |
dc.identifier.scopusid | 2-s2.0-84983315657 | - |
dc.citation.title | NATURE COMMUNICATIONS | - |
dc.citation.volume | 7 | - |
dc.contributor.affiliatedAuthor | Park, Chul-Kyu | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | PRIMARY SENSORY NEURONS | - |
dc.subject.keywordPlus | NEUROPATHIC PAIN | - |
dc.subject.keywordPlus | INFLAMMATORY PAIN | - |
dc.subject.keywordPlus | DORSAL-HORN | - |
dc.subject.keywordPlus | PERIPHERAL NEUROPATHY | - |
dc.subject.keywordPlus | CENTRAL SENSITIZATION | - |
dc.subject.keywordPlus | MECHANICAL ALLODYNIA | - |
dc.subject.keywordPlus | NOCICEPTIVE NEURONS | - |
dc.subject.keywordPlus | SYNAPTIC PLASTICITY | - |
dc.subject.keywordPlus | MORPHINE-TOLERANCE | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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