Elmas, PinarUlugol, Ahmet2024-06-122024-06-1220130300-95641435-1463https://doi.org/10.1007/s00702-013-1052-7https://hdl.handle.net/20.500.14551/20518Cannabinoid CB1 receptors have been implicated in the antinociceptive effect of paracetamol. In the current study, we examined whether blockade of CB1 receptors prevent the analgesic activity of dipyrone, in a similar way to paracetamol. Hot-plate and tail-flick tests were used to assess the antinociceptive activity in mice. Dipyrone and WIN 55,212-2, a cannabinoid agonist, exerted significant antinociceptive effects in both hot-plate and tail flick tests. The CB1 receptor antagonist, AM-251 (3 mg/kg), at a dose which had no effect when used alone, did not alter the antinociceptive effect of dipyrone, whereas completely prevented the antinociceptive activity of WIN 55,212-2 in both thermal antinociceptive tests. Our findings suggest that, unlike paracetamol, cannabinoid CB1 receptors do not participate in the antinociceptive action of dipyrone when acute pain tests used.en10.1007/s00702-013-1052-7info:eu-repo/semantics/closedAccessDipyroneWIN 55,212-2CB1 ReceptorAntinociceptionPag-Microinjected DipyroneEndogenous OpioidsSpinal-CordRvm AxisMetamizolRatsMicePainParacetamolActivationArticle1201115331538Q2WOS:0003260549000032-s2.0-8488724470923784345Q2