Article
- The EMBO Journal (2001) 20, 2349 - 2356
- doi:10.1093/emboj/20.10.2349
Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N-type Ca2+ channel
Hironao Saegusa1,2, Takashi Kurihara1,2, Shuqin Zong1, An-a Kazuno1, Yoshihiro Matsuda1, Takahiro Nonaka1, Wenhua Han1, Hideyuki Toriyama1 and Tsutomu Tanabe1
- Department of Pharmacology and Neurobiology, Graduate School of Medicine, Tokyo Medical and Dental University and CREST, Japan Science and Technology Corporation, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
- H.Saegusa and T.Kurihara contributed equally to this work
Correspondence to:
Tsutomu Tanabe, E-mail: t-tanabe.mphm@tmd.ac.jp
Received 20 November 2000; Accepted 19 March 2001; Revised 15 March 2001
Abstract
The importance of voltage-dependent Ca2+ channels (VDCCs) in pain transmission has been noticed gradually, as several VDCC blockers have been shown to be effective in inhibiting this process. In particular, the N-type VDCC has attracted attention, because inhibitors of this channel are effective in various aspects of pain-related phenomena. To understand the genuine contribution of the N-type VDCC to the pain transmission system, we generated mice deficient in this channel by gene targeting. We report here that mice lacking N-type VDCCs show suppressed responses to a painful stimulus that induces inflammation and show markedly reduced symptoms of neuropathic pain, which is caused by nerve injury and is known to be difficult to treat by currently available therapeutic methods. This finding clearly demonstrates that the N-type VDCC is essential for development of neuropathic pain and, therefore, controlling the activity of this channel can be of great importance for the management of neuropathic pain.
Keywords:
- Cav2.2,
- gene targeting,
- N-type calcium channel,
- pain
