Repeated morphine treatment-mediated hyperalgesia, allodynia and spinal glial activation are blocked by co-administration of a selective cannabinoid receptor type-2 agonist

详细信息	查看全文 | 推荐本文 |

• 作者：Suneeta Tumati^a ; Tally M. Largent-Milnes^a ; Attila Keresztes^a ; Jiyang Ren^a ; William R. Roeske^a ; ^c ; ^e ; Todd W. Vanderah^a ; ^b ; Eva V. Varga^a ; ^d ; ^e ; ^{evarga@email.arizona.edu}
• 关键词：AM 1241 ; (3-iodo-5-nitrophenyl)-[1-[(1-methylpiperidin-2-yl)methyl]indol-3-yl]methanone ; i.p. ; intraperitoneal ; Isoflurane ; 2-chloro-2-(difluoromethoxy)-1 ; 1 ; 1-trifluoro-ethane ; AM 251 ; 1-(2 ; 4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-(1-piperidyl)pyrazo
• 刊名：Journal of Neuroimmunology
• 出版年：2012
• 期刊代码：32_01655728
• 类别：neu
• 出版时间：March, 2012
• 卷：244
• 期：1-2
• 页码：23-31
• 文件大小：1412 K

摘要

Spinal glial activation has been implicated in sustained morphine-mediated paradoxical pain sensitization. Since activation of glial CB2 cannabinoid receptors attenuates spinal glial activation in neuropathies, we hypothesized that CB2 agonists may also attenuate sustained morphine-mediated spinal glial activation and pain sensitization. Our data indicate that co-administration of a CB2-selective agonist (AM 1241) attenuates morphine (intraperitoneal; twice daily; 6 days)-mediated thermal hyperalgesia and tactile allodynia in rats. A CB2 (AM 630) but not a CB1 (AM 251) antagonist mitigated this effect. AM 1241 co-treatment also attenuated spinal astrocyte and microglial marker and pro-inflammatory mediator (IL-1尾, TNF伪) immunoreactivities in morphine-treated rats, suggesting that CB2 agonists may be useful to prevent the neuroinflammatory consequences of sustained morphine treatment.