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Induction of CB2 receptor expression in the rat spinal cord of neuropathic but not inflammatory chronic pain models
Author(s) -
Zhang Ji,
Hoffert Cyrla,
Vu Huy Khang,
Groblewski Thierry,
Ahmad Sultan,
O'Donnell Dajan
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02704.x
Subject(s) - neuropathic pain , chronic pain , medicine , spinal cord , cannabinoid receptor type 2 , microglia , receptor , nociception , inflammation , analgesic , pharmacology , neuroscience , immune system , cannabinoid receptor , immunology , biology , agonist , physical therapy , psychiatry
Cannabinoids have been considered for some time as potent therapeutic agents in chronic pain management. Central and systemic administration of natural, synthetic and endogenous cannabinoids produce antinociceptive and antihyperalgesic effects in both acute and chronic animal pain models. Although much of the existing data suggest that the analgesic effects of cannabinoids are mediated via neuronal CB1 receptors, there is increasing evidence to support a role for peripheral CB2 receptors, which are expressed preferentially on immune cells. As yet, little is known about the central contribution of CB2 in neuropathic pain states. We report here that chronic pain models associated with peripheral nerve injury, but not peripheral inflammation, induce CB2 receptor expression in a highly restricted and specific manner within the lumbar spinal cord. Moreover, the appearance of CB2 expression coincides with the appearance of activated microglia.