Abstract

The present study investigated the effect of per oral (p.o.) administration of butyl (2-phenylethynyl) selenide (1-50mg/kg) on formalin-induced nociception in mice. The involvement of serotonergic, adenosinergic, muscarinic cholinergic and opioid mechanisms in the antinociceptive effect was also investigated. Butyl (2-phenylethynyl) selenide inhibited both neurogenic (at doses equal or higher than 10mg/kg) and inflammatory (at doses equal or higher than 25mg/kg) phases of the nociception caused by intraplantar (i.pl.) injection of 2.5% formalin solution (20 microl), with ID(50) values of 36.7 (29.28-46.0) and 20.37 (15.74-26.36) mg/kg, respectively. This compound reduced the formalin-induced paw oedema formation (55 + or - 4%) at doses equal or higher than 25mg/kg. The antinociceptive effect of compound (25mg/kg, p.o.) was reversed by ondansetron (0.5mg/kg, a 5-HT(3) receptor antagonist) and caffeine (3mg/kg, a nonselective adenosine receptor antagonist), but not by atropine (0.1mg/kg, a non selective muscarinic antagonist), WAY100635 (0.1mg/kg, a selective 5-HT(1A) receptor antagonist), ritanserin (1mg/kg, a 5-HT(2) receptor antagonist) and naloxone (1mg/kg, a non selective opioid receptor antagonist). These results indicate that butyl (2-phenylethynyl) selenide produced antinociception in the formalin test through mechanisms that involve an interaction with serotonergic (5-HT(3)) and adenosinergic systems.

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