• Simone Monaliza S Lamana, Marcelo H Napimoga, Ana Paula Camatta Nascimento, Fabiana F Freitas, Daniele R de Araujo, Mariana S Quinteiro, Cristina G Macedo, Carlos L Fogaça, and Juliana T Clemente-Napimoga.
• Department of Physiological Sciences, Laboratory of Orofacial Pain, Piracicaba Dental School, University of Campinas - UNICAMP, Piracicaba, SP, Brazil.
• Eur. J. Pharmacol. 2017 Jul 15; 807: 82-90.

AbstractTramadol is a centrally acting analgesic drug able to prevent nociceptor sensitization when administered into the temporomandibular joint (TMJ) of rats. The mechanism underlying the peripheral anti-inflammatory effect of tramadol remains unknown. This study demonstrated that intra-TMJ injection of tramadol (500µg/TMJ) was able to inhibit the nociceptive response induced by 1.5% formalin or 1.5% capsaicin, suggesting that tramadol has an antinociceptive effect, acting directly on the primary nociceptive neurons activating the nitric oxide/cyclic guanosine monophosphate signaling pathway. Tramadol also inhibited the nociceptive response induced by carrageenan (100µg/TMJ) or 5-hydroxytryptamine (225µg/TMJ) along with inhibition of inflammatory cytokines levels, leukocytes migration and plasma extravasation. In conclusion, the results demonstrate that peripheral administration of tramadol has a potential antinociceptive and anti-inflammatory effect. The antinociceptive effect is mediated by activation of the intracellular nitric oxide/cyclic guanosine monophosphate pathway, at least in part, independently from the opioid system.Copyright © 2017 Elsevier B.V. All rights reserved.

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