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J. Biol. Chem., Vol. 282, Issue 7, 4757-4764, February 16, 2007

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Molecular Basis of Ca_v2.3 Calcium Channels in Rat Nociceptive Neurons^*

Zhi Fang¹, Chul-Kyu Park¹, Hai Ying Li, Hyun Yeong Kim, Seong-Hae Park, Sung Jun Jung, Joong Soo Kim, Arnaud Monteil^¶, Seog Bae Oh², and Richard J. Miller^||

From the Department of Physiology and Program in Molecular and Cellular Neuroscience, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 110-749, Korea, the Department of Physiology, College of Medicine, Kangwon National University, Chunchon 200-710, Korea, the ^¶Département de Physiologie, Institut de Génomique Fonctionnelle, CNRS-UMR 5203 141, Rue de la Cardonille 34396 Montpellier Cedex 5, France, and the ^||Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611

Ca_v2.3 calcium channels play an important role in pain transmission in peripheral sensory neurons. Six Ca_v2.3 isoforms resulting from different combinations of three inserts (inserts I and II in the II–III loop and insert III in the carboxyl-terminal region) have been identified in different mammalian tissues. To date, however, Ca_v2.3 isoforms unique to primary sensory neurons have not been identified. In this study, we determined Ca_v2.3 isoforms expressed in the rat trigeminal ganglion neurons. Whole tissue reverse transcription (RT)-PCR analyses revealed that only two isoforms, Ca_v2.3a and Ca_v2.3e, are present in TG neurons. Using single cell RT-PCR, we found that Ca_v2.3e is the major isoform, whereas Ca_v2.3e expression is highly restricted to small (<16 µm) isolectin B4-negative and tyrosine kinase A-positive neurons. Ca_v2.3e was also preferentially detected in neurons expressing the nociceptive marker, transient receptor potential vanilloid 1. Single cell RT-PCR following calcium imaging and whole-cell patch clamp recordings provided evidence of an association between an R-type calcium channel component and Ca_v2.3e expression. Our results suggest that Ca_v2.3e in sensory neurons may be a potential target for the treatment of pain.

Received for publication, June 1, 2006 , and in revised form, November 27, 2006.

^* This work was supported by MOEHRD Grant KRF-2003-003-E00207 from the Korea Research Foundation, Grant R01-2004-000-10384-0 from the Basic Research Program of the Korea Science and Engineering Foundation, and Grant M103KV010015-06K2201-01510 from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, Republic of Korea. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Both authors contributed equally to this work.

² To whom correspondence should be addressed. Tel.: 82-2-740-8656; Fax: 82-2-762-5107; E-mail: odolbae{at}snu.ac.kr.

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