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Neuroscience. 2014 Mar 7;261:153-60. doi: 10.1016/j.neuroscience.2013.12.047. Epub 2013 Dec 30.

Activation of transient receptor potential ankyrin 1 by eugenol.

Author information

1
Dental Research Institute and Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul, Republic of Korea; Pain Cognitive Function Research Center, Seoul National University, Seoul, Republic of Korea.
2
Dental Research Institute and Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul, Republic of Korea.
3
Pain Cognitive Function Research Center, Seoul National University, Seoul, Republic of Korea; Department of Physiology, College of Medicine, Hanyang University, Seoul, Republic of Korea.
4
Division of Metabolism and Functionality Research, Korea Food Research Institute, Sungnam, Republic of Korea.
5
Dental Research Institute and Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul, Republic of Korea; Pain Cognitive Function Research Center, Seoul National University, Seoul, Republic of Korea; Department of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul, Republic of Korea. Electronic address: odolbae@snu.ac.kr.

Abstract

Eugenol is a bioactive plant extract used as an analgesic agent in dentistry. The structural similarity of eugenol to cinnamaldehyde, an active ligand for transient receptor potential ankyrin 1 (TRPA1), suggests that eugenol might produce its effect via TRPA1, in addition to TRPV1 as we reported previously. In this study, we investigated the effect of eugenol on TRPA1, by fura-2-based calcium imaging and patch clamp recording in trigeminal ganglion neurons and in a heterologous expression system. As the result, eugenol induced robust calcium responses in rat trigeminal ganglion neurons that responded to a specific TRPA1 agonist, allyl isothiocyanate (AITC), and not to capsaicin. Capsazepine, a TRPV1 antagonist failed to inhibit eugenol-induced calcium responses in AITC-responding neurons. In addition, eugenol response was observed in trigeminal ganglion neurons from TRPV1 knockout mice and human embryonic kidney 293 cell lines that express human TRPA1, which was inhibited by TRPA1-specific antagonist HC-030031. Eugenol-evoked TRPA1 single channel activity and eugenol-induced TRPA1 currents were dose-dependent with EC50 of 261.5μM. In summary, these results demonstrate that the activation of TRPA1 might account for another molecular mechanism underlying the pharmacological action of eugenol.

KEYWORDS:

AITC; TRPA1; analgesia; eugenol; pain; trigeminal ganglion

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