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

Suneeta Tumati, Tally M. Largent-Milnes, Attila Keresztes, Jiyang Ren, William R. Roeske, Todd W. Vanderah, Eva V. Varga

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)23-31
Number of pages9
JournalJournal of Neuroimmunology
Volume244
Issue number1-2
DOIs
StatePublished - Mar 1 2012

Keywords

  • Allodynia
  • CB2 agonist
  • Hyperalgesia
  • Morphine
  • Pain sensitization
  • Spinal glia

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Fingerprint Dive into the research topics of 'Repeated morphine treatment-mediated hyperalgesia, allodynia and spinal glial activation are blocked by co-administration of a selective cannabinoid receptor type-2 agonist'. Together they form a unique fingerprint.

Cite this