Eugenol Inhibits Sodium Currents in Dental Afferent Neurons
C.-K. Park1,
,
H.Y. Li1,,
K.-Y. Yeon1,
S.J. Jung2,
S.-Y. Choi1,
S.J. Lee1,
S. Lee3,
K. Park1,
J.S. Kim1, and
S.B. Oh1,*
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
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Figure 1. Effect of eugenol on action potentials in dental primary afferent neurons. At –65 mV, action potentials were evoked with 5-ms depolarizing current pulses with increasing amplitude (0.2 ~ 1 nA in 50.0-pA steps). Dental primary afferent neurons were classified into two types based on action potential shape: (A) The chemical structures of eugenol and capsaicin. Eugenol shares the vanilloid-moiety with capsaicin. (B) Type I neurons that had a prominent shoulder in the falling phase of the action potential were inhibited by capsaicin (n = 15). (C) Type II neurons that had no hump in the falling phase of the action potential were not affected by capsaicin (n = 15). Eugenol inhibited the generation of action potentials in both types of dental primary afferent neurons. B and C are representative responses of type I and type II neurons, respectively.
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Figure 2. Effect of eugenol on voltage-gated sodium channel currents (INa) in dental primary afferent neurons. (Aa) Time-course of the effects of eugenol (1 mM) and capsaicin (1 µM) on INa in a capsaicin-insensitive neuron. Eugenol (1 mM) inhibited INa in capsaicin-insensitive neurons (n = 20). (Ab) Superimposed INa evoked by a test pulse at the points indicated in Aa. (Ba) The INa inhibition by eugenol was also observed in capsaicin-sensitive neurons (n = 30). (Bb) Superimposed INa evoked by a test pulse at the points indicated in Ba. A and B are representative traces illustrating the effect of eugenol on INa from capsaicin-insensitive and capsaicin-sensitive neurons, respectively. (C) Dose-response relationship of eugenol-induced INa inhibition. The inhibition of the peak INa by eugenol was dose-dependent with IC50 of 600 µM. (Da) The summary of INa inhibition in dental primary afferent neurons. Eugenol (1 mM)-induced INa inhibition in capsaicin-sensitive neurons (Cap-S) was similar to that obtained in capsaicin-insensitive neurons (Cap-Ins). (Db) The effect of capsazepine (10 µM), a competitive TRPV1 antagonist, on eugenol-induced INa inhibition. The INa inhibition by combined application of eugenol and capsazepine was not significantly different from that of eugenol (mean ± SEM, p > 0.05), indicating that eugenol-induced INa inhibition was TRPV1-independent. The numbers in parentheses represent the number of cells studied.
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Figure 3. Effect of eugenol on two types of INa in dental primary afferent neurons. Both TTX-sensitive (TTX-s) and TTX-resistant (TTX-r) INa were present in dental primary afferent neurons. (Aa) TTX-r INa was predominant in small neurons (< 25 µm). TTX-s INa is the difference current of total INa and TTX-r INa. (Ab) TTX-r INa was blocked by 1 mM eugenol (n = 7). (B) TTX-s INa, which was predominant in large neurons (> 35 µm), was also blocked by 1 mM eugenol (n = 5). A and B are representative traces illustrating the effect of eugenol from TTX-r and TTX-s neurons, respectively. (C) The summary of TTX-r INa and TTX-s INa inhibition in dental primary afferent neurons. The extent of inhibition by eugenol on TTX-r INa was similar to that on TTX-s INa (mean ± SEM, p > 0.01). The numbers in parentheses represent the number of cells studied.
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