CB2 receptor protein and mRNA expression in dorsal root ganglia of two rat neuropathic pain models.
|Fakulta / Pracoviště MU|
|Popis||Agonists of cannabinoid receptors (CB1R and CB2R) modulate nociceptive signal transmission and seem to be promising in treatment of neuropathic pain. Importantly, CB2R activation inhibits pain responses without adverse, most often psychotropic effects that are produced by CB1R agonists. CB2R synthesis and protein distribution of protein in the dorsal root ganglia (DRG) were investigated using immunohistochemistry and in situ hybridization in two rat neuropathic pain models– chronic constriction injury (CCI) and spared nerve injury (SNI). Both types of nerve injury induced symptoms of neuropathic pain which were measured as a decrease of paw withdrawal threshold (mechanical allodynia) and withdrawal latency (thermal hyperalgesia). CCI and SNI resulted in up-regulation of CB2R in both neurons and satellite glial cells of the rat DRG related to injury. Unilateral nerve injuries always induced bilateral increase of both CB2R protein and mRNA comparing with sham-operated animals. Bilateral CB2R up-regulation was found not only in DRG associated with damaged nerve but also in those of spinal cord segments remote from the operation (C7, C8 levels). Increased CB2R protein in DRG of both neuropathic pain models was confirmed by expression of CB2R mRNA using in situ hybridization.|