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Modulation of Ca_V2.3 Calcium Channel Currents by Eugenol

¹ Department of Physiology, School of Dentistry and Dental Research Institute, 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

Eugenol, a natural congener of capsaicin, is a routine analgesic agent in dentistry. We have recently demonstrated the inhibition of Ca_V2.2 calcium channel and sodium channel currents to be molecular mechanisms underlying the analgesic effect of eugenol. We hypothesized that Ca_V2.3 channels are also modulated by eugenol and investigated its mode of action using the whole-cell patch-clamp technique in a heterologous expression system. Eugenol inhibited calcium currents in the E52 cell line, stably expressing the human Ca_V2.3 calcium channels, where TRPV1 is not endogenously expressed. The extent of current inhibition was not significantly different between naïve E52 cells and TRPV1-expressing E52 cells, suggesting no involvement of TRPV1. In contrast, TRPV1 activation is prerequisite for the inhibition of Ca_V2.3 calcium channels by capsaicin. The results indicate that eugenol has mechanisms distinct from those of capsaicin for modulating Ca_V2.3 channels. We suggest that inhibition of Ca_V2.3 channels by eugenol might contribute to its analgesic effect.

KEY WORDS: eugenol • voltage-gated calcium channels • Ca_V2.3 • R-type calcium channels