Attenuated Neuropathic Pain in Ca(V)3.1 Null Mice

To assess the role of α1G T-type Ca2+ channels in neuropathic pain after L5 spinal nerve ligation, we examined behavioral pain susceptibility in mice lacking CaV3.1 (α1G −/−), the gene encoding the pore-forming units of these channels. Reduced spontaneous pain responses and an increased threshold fo...

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Published inMolecules and cells pp. 242 - 246
Main Authors 나흥식, Soonwook Choi, 김준선, Joonoh Park, 신희섭
Format Journal Article
LanguageEnglish
Published 한국분자세포생물학회 30.04.2008
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Summary:To assess the role of α1G T-type Ca2+ channels in neuropathic pain after L5 spinal nerve ligation, we examined behavioral pain susceptibility in mice lacking CaV3.1 (α1G −/−), the gene encoding the pore-forming units of these channels. Reduced spontaneous pain responses and an increased threshold for paw withdrawal in response to mechanical stimulation were observed in these mice. The α1G −/− mice also showed attenuated thermal hyperalgesia in response to both low-(IR30) and high-intensity (IR60) infrared stimulation. Our results reveal the importance of α1G T-type Ca2+ channels in the development of neuropathic pain, and suggest that selective modulation of α1G subtype channels may provide a novel approach to the treatment of allodynia and hyperalgesia. KCI Citation Count: 42
Bibliography:G704-000079.2008.25.2.023
ISSN:1016-8478
0219-1032