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...
Saved in:
Published in | Molecules and cells pp. 242 - 246 |
---|---|
Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
한국분자세포생물학회
30.04.2008
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
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 |