Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N-type Ca2+ channel

The importance of voltage-dependent Ca2+ channels (VDCCs) in pain transmiss ion has been noticed gradually, as several VDCC blockers have been shown to be effective in inhibiting this process, In particular, the N-type VDCC ha s attracted attention, because inhibitors of this channel are effective in various aspects of pain-related phenomena. To understand the genuine contri bution of the N-type VDCC to the pain transmission system, we generated mic e deficient in this channel by gene targeting. We report here that mice lac king N-type VDCCs show suppressed responses to a painful stimulus that indu ces inflammation and show markedly reduced symptoms of neuropathic pain, wh ich is caused by nerve injury and is known to be difficult to treat by curr ently available therapeutic methods. This finding clearly demonstrates that the N-type VDCC is essential for development of neuropathic pain and, ther efore, controlling the activity of this channel can be of great importance for the management of neuropathic pain.