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J Neuroimmunol. 2012 Mar;244(1-2):23-31. doi: 10.1016/j.jneuroim.2011.12.021. Epub 2012 Jan 30.

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

Author information

1
Department of Pharmacology, The University of Arizona, Tucson, AZ 85724, USA.

Abstract

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-1β, TNFα) immunoreactivities in morphine-treated rats, suggesting that CB2 agonists may be useful to prevent the neuroinflammatory consequences of sustained morphine treatment.

PMID:
22285397
PMCID:
PMC3298577
DOI:
10.1016/j.jneuroim.2011.12.021
[Indexed for MEDLINE]
Free PMC Article

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