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Eugenol Inhibits Sodium Currents in Dental Afferent Neurons

C.-K. Park^1,, H.Y. Li^1,, K.-Y. Yeon¹, S.J. Jung², S.-Y. Choi¹, S.J. Lee¹, S. Lee³, K. Park¹, J.S. Kim¹, and S.B. Oh^1,*

¹ Department of Physiology and
³ Program in Molecular and Cellular Neuroscience, College of Dentistry and Dental Research Institute, BK21 Program, Seoul National University, 28-2 Yeongeon-Dong Chongno-Ku, Seoul 110-749, Korea; and
² Department of Physiology, College of Medicine, Kangwon National University, Chunchon 200-710, Korea

^* corresponding author, odolbae{at}snu.ac.kr

Although eugenol is widely used in dentistry, little is known about the molecular mechanisms responsible for its anesthetic properties. In addition to calcium channels, recently demonstrated by our group, there could be another molecular target for eugenol. Using a whole-cell patch-clamp technique, we investigated the effect of eugenol on voltage-gated sodium channel currents (I_Na) in rat dental primary afferent neurons identified by retrograde labeling with a fluorescent dye in maxillary molars. Eugenol inhibited action potentials and I_Na in both capsaicin-sensitive and capsaicin-insensitive neurons. The pre-treatment with capsazepine, a competitive antagonist of transient receptor potential vanilloid 1 (TRPV1), failed to block the inhibitory effect of eugenol on I_Na, suggesting no involvement of TRPV1. Two types of I_Na, tetrodotoxin (TTX)-resistant and TTX-sensitive I_Na, were inhibited by eugenol. Our results demonstrated that eugenol inhibits I_Na in a TRPV1-independent manner. We suggest that I_Na inhibition by eugenol contributes to its analgesic effect.

KEY WORDS: eugenol • trigeminal ganglion neurons • voltage-gated sodium channels

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