Authors:
Costa B, Giagnoni G, Franke C, Trovato AE, Colleoni M.
Abstract:
Cannabidiol (CBD), a nonpsychoactive marijuana constituent, was recently
shown as an oral antihyperalgesic compound in a rat model of acute
inflammation. We examined whether the CBD antihyperalgesic effect could
be mediated by cannabinoid receptor type 1 (CB1) or cannabinoid receptor
type 2 (CB2) and/or by transient receptor potential vanilloid type 1
(TRPV1). Rats received CBD (10 mg kg(-1)) and the selective antagonists:
SR141716
(N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide)
for CB1, SR144528
(N-[(1S)-endo-1,3,3-trimethylbicyclo[2.2.1]heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)pyrazole-3
carboxamide) for CB2 and capsazepine (CPZ) for TRPV1 receptors. The
intraplantar injection of carrageenan in rats induced a time-dependent
thermal hyperalgesia, which peaked at 3 h and decreased at the following
times. CBD, administered 2 h after carrageenan, abolished the
hyperalgesia to the thermal stimulus evaluated by plantar test. Neither
SR141716 (0.5 mg kg(-1)) nor SR144528 (3 and 10 mg kg(-1)) modified the
CBD-induced antihyperalgesia; CPZ partially at the lowest dose (2 mg
kg(-1)) and fully at the highest dose (10 mg kg(-1)) reversed this
effect. These results demonstrate that TRPV1 receptor could be a
molecular target of the CBD antihyperalgesic action.