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Molecular mechanism for local anesthetic action of eugenol in the rat trigeminal system

Park, Chul-Kyua; Kim, Kihwana; Jung, Sung Junb; Kim, Min Jic; Ahn, Dong Kukc; Hong, Seong-Dood; Kim, Joong Sooa; Oh, Seog Baea,*

doi: 10.1016/j.pain.2009.03.016
Articles

ABSTRACT Eugenol is widely used in dentistry as a local analgesic agent, because of its ability to allay tooth pain. Interestingly, eugenol shares several pharmacological actions with local anesthetics which include inhibition of voltage-gated sodium channel (VGSC) and activation of transient receptor potential vanilloid subtype 1 (TRPV1). In the present study, we investigated the effects of eugenol on pain behaviors in orofacial area, and as an attempt to elucidate its mechanism we characterized inhibitory effects of eugenol on VGSCs in trigeminal ganglion (TG) neurons. TG neurons were classified into four types on the basis of their neurochemical and electrophysiological properties such as cell size, shapes of action potential (AP), isolectin-B4 (IB4) binding, and were analyzed for the association of their distinctive electrophysiological properties and mRNA expression of Nav1.8 and TRPV1 by using single-cell RT-PCR following whole-cell recordings. Subcutaneous injection of eugenol reduced the thermal nociception and capsaicin-induced thermal hyperalgesia in a dose-dependent manner. Eugenol also diminished digastric electromyogram evoked by noxious electrical stimulation to anterior tooth pulp, which was attributable to the blockade of AP conduction on inferior alveolar nerve. At cellular level, eugenol reversibly inhibited APs and VGSCs in IB4+/TRPV1+/Nav1.8+ nociceptive TG neurons (Type I–Type III) and IB4−/TRPV1−/Nav1.8− nociceptive TG neurons (Type IV). Both TTX-resistant INa in Type I–Type III neurons and TTX-sensitive INa in Type IV neurons were sensitive to eugenol. Taken together, these results suggest that eugenol may serve as local anesthetics for other pathological pain conditions in addition to its wide use in dental clinic.

a National Research Laboratory for Pain, Dental Research Institute and Department of Physiology, School of Dentistry, Seoul National University, 28-2 Yeongeon-Dong, Chongno-Ku, Seoul 110-749, Republic of Korea

b Department of Physiology, College of Medicine, Kangwon National University, Chunchon 200-710, Republic of Korea

c Department of Oral Physiology and Neurobiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Republic of Korea

d Department of Oral Pathology, School of Dentistry, Seoul National University, Seoul 110-749, Republic of Korea

*Corresponding author. Tel.: +82 2 740 8656; fax: +82 2 762 5107.

E-mail address: odolbae@snu.ac.kr

ARTICLE INFO

Article history:

Received October 14, 2008

Received in revised form February 4, 2009

Accepted March 16, 2009.

© 2009 Lippincott Williams & Wilkins, Inc.
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