Abstract | BACKGROUND: METHODS: RESULTS: Incision and remifentanil induced mechanical allodynia, heat hyperalgesia, and cold hyperalgesia accompanied by upregulated P2Y1R expression, increased NMDAR subunit NR1 expression and phosphorylation at Ser896, and NR2B expression and phosphorylation at Tyr1472 in DRG. Inhibition of NMDAR phosphorylation by MK801 effectively attenuated remifentanil-induced postoperative hyperalgesia. Furthermore, P2Y1R blockade by MRS2179 not only lessened remifentanil-evoked postoperative hypersensitivity to mechanical, heat, and cold stimuli, but also suppressed the increases in NR1 and NR2B expression and phosphorylation in DRG induced by incision and remifentanil. CONCLUSION: The process by which P2Y1R mediates NMDAR expression and phosphorylation represents a mechanism of remifentanil-induced postoperative hyperalgesia in the DRG and/or spinal cord.
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Authors | Lin Su, Xiaoqing Bai, Tongxiang Niu, Xinqi Zhuang, Beibei Dong, Guolin Wang, Yonghao Yu |
Journal | Brain research bulletin
(Brain Res Bull)
Vol. 177
Pg. 352-362
(12 2021)
ISSN: 1873-2747 [Electronic] United States |
PMID | 34653560
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2021 Elsevier Inc. All rights reserved. |
Chemical References |
- Piperidines
- Receptors, N-Methyl-D-Aspartate
- Receptors, Purinergic P2Y1
- Remifentanil
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Topics |
- Animals
- Ganglia, Spinal
(metabolism)
- Hyperalgesia
(chemically induced, drug therapy, metabolism)
- Pain, Postoperative
(chemically induced, drug therapy, metabolism)
- Phosphorylation
- Piperidines
(pharmacology)
- Rats
- Rats, Sprague-Dawley
- Receptors, N-Methyl-D-Aspartate
(metabolism)
- Receptors, Purinergic P2Y1
(metabolism)
- Remifentanil
(adverse effects)
- Spinal Cord
(metabolism)
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