Attenuated pain responses in mice lacking CaV3.2 T-type channels

Authors

  • S. Choi,

    1. Center for Neural Science, Division of Life Sciences, Korea Institute of Science and Technology, Seoul, Korea
    2. Department of Neuroscience, University of Science and Technology, Daejon, Korea
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    • ††

      Two authors equally contributed to this work.

  • H. S. Na,

    1. Department of Physiology, Korea University, College of Medicine, Seoul, Korea
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    • ††

      Two authors equally contributed to this work.

  • J. Kim,

    1. Department of Physiology, Korea University, College of Medicine, Seoul, Korea
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  • J. Lee,

    1. Center for Neural Science, Division of Life Sciences, Korea Institute of Science and Technology, Seoul, Korea
    2. Department of Neuroscience, University of Science and Technology, Daejon, Korea
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  • S. Lee,

    1. Center for Neural Science, Division of Life Sciences, Korea Institute of Science and Technology, Seoul, Korea
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  • D. Kim,

    1. Center for Neural Science, Division of Life Sciences, Korea Institute of Science and Technology, Seoul, Korea
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    • ‡‡

      Present address: Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejon 305-701, Korea.

  • J. Park,

    1. Center for Neural Science, Division of Life Sciences, Korea Institute of Science and Technology, Seoul, Korea
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  • C.-C. Chen,

    1. Howard Hughes Medical Institute, Department of Physiology & Biophysics, University of Iowa, Iowa City, IA
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    • §§

      Present address: Institute of Biomedical Sciences, Academia Sinica, 128 Academia Rd, Nankang, Taipei 115, Taiwan.

  • K. P. Campbell,

    1. Howard Hughes Medical Institute, Department of Physiology & Biophysics, University of Iowa, Iowa City, IA
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  • H.-S. Shin

    Corresponding author
    1. Center for Neural Science, Division of Life Sciences, Korea Institute of Science and Technology, Seoul, Korea
    2. Department of Neuroscience, University of Science and Technology, Daejon, Korea
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Hee-Sup Shin, 39-1 Hawolgok-dong, Seongbuk-gu, Center for Neural Science, Korea Institute of Science and Technology, Seoul 136-791, Korea. E-mail: shin@kist.re.kr

Abstract

Although T-type Ca2+ channels are implicated in nociception, the function of specific subtypes has not been well defined. Here, we compared pain susceptibility in mice lacking CaV3.2 subtype of T-type Ca2+ channels (CaV3.2−/−) with wild-type littermates in various behavioral models of pain to explore the roles of CaV3.2 in the processing of noxious stimuli in vivo. In acute mechanical, thermal and chemical pain tests, CaV3.2−/− mice showed decreased pain responses compared to wild-type mice. CaV3.2−/− mice also displayed attenuated pain responses to tonic noxious stimuli such as intraperitoneal injections of irritant agents and intradermal injections of formalin. In spinal nerve ligation-induced neuropathic pain, however, behavioral responses of CaV3.2−/− mice were not different from those of wild-type mice. The present study reveals that the CaV3.2 subtype of T-type Ca2+ channels are important in the peripheral processing of noxious signals, regardless of modality, duration or affected tissue type.

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