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- Suneeta Tumati, Tally M Largent-Milnes, Attila Keresztes, Jiyang Ren, William R Roeske, Todd W Vanderah, and Eva V Varga.
- Department of Pharmacology, The University of Arizona, Tucson, AZ 85724, USA.
- J. Neuroimmunol. 2012 Mar 1; 244 (1-2): 23-31.
AbstractSpinal 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-1β, TNFα) immunoreactivities in morphine-treated rats, suggesting that CB2 agonists may be useful to prevent the neuroinflammatory consequences of sustained morphine treatment.Published by Elsevier B.V.
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