Resumo

Introduction: The voltage-sensitive calcium channels (VSCCs) play a key role in several cellular and physiological functions like neurotransmitter release from both central and peripheral nerves. Phoneutria nigriventer toxins have shown a high potential to block these channels and one of these toxins, Tx3-4 blocks P/Q-type of VSCCs (Miranda et al, 2001). The present study investigates the Tx3-4 action on the inflammatory nociception. Methods: Experimental Animal Ethics Committee: 4201092005-6. Tests of behavior were performed on healthy Swiss mice (25-35 g) injecting intrathecally (i.t.) 5 ìl of Tx3-4 (3-30 pmol/site) or omega-conotoxin MVIIC (3-30 pmol/site) , a control toxin, 0.5 h, 1h, 2h, and 3 hours before injection of formalin (2,5% formaldehyde in saline, 20 ìl volume) into the plantar surface of the right hind paw. Tx3-4 and MVIIC (3 pmol/site) were administrated 0.25 to 4 h after plantar surface incision into the plantar surface of the right hind paw. The injected hind paw pain behavior’s time and the postoperative mechanical allodynia were measured in the formalin test and incisional pain model, respectively. Results: The phonotoxin intratecally injected (30 pmol/site) presented an antinociceptive effect of 60± 8% , 1 hour before formalin administration (P < 0.05 compared with “placebo” treatment) and an antinociceptive effect of 80±12% , 1 h after plantar incision (P < 0.001 compared with vehicle). The MVIIC did not present antinociceptive activity on first test but inhibited 65±10% of allodynia 1 h after paw surgery (P < 0.01 compared with vehicle). Discussion and Conclusion: The Tx3-4 toxin presented an antinociceptive effect on inflammatory nociceptive models. It was able to inhibit formalin induced nociception in pre-treatment and inhibited postoperative mechanical allodynia, and as so, it has been more powerfull and effective in clinic model. Thus, more studies are necessary to better clarify the mechanisms involved in the Tx3-4 antinociceptive spinal activity.