Attenuated neuropathic pain in Cav3.1 null mice.
To assess the role of alpha(1G) T-type Ca2+ channels in neuropathic pain after L5 spinal nerve ligation, we examined behavioral pain susceptibility in mice lacking CaV3.1 (alpha1G(-/-)), 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 alpha1G(-/-) mice also showed attenuated thermal hyperalgesia in response to both low-(IR30) and high-intensity (IR60) infrared stimulation. Our results reveal the importance of alpha(1G) T-type Ca2+ channels in the development of neuropathic pain, and suggest that selective modulation of alpha1G subtype channels may provide a novel approach to the treatment of allodynia and hyperalgesia.
Na
Heung Sik
HS
Center for Neural Science, Korea Institute of Science and Technology, Seoul 136-791, Korea.
Choi
Soonwook
S
Kim
Junesun
J
Park
Joonoh
J
Shin
Hee-Sup
HS
D000818:Animals; D020747:Calcium Channels, T-Type / Q000172:deficiency* / Q000378:metabolism; D007259:Infrared Rays; D051379:Mice; D008810:Mice, Inbred C57BL; D009437:Neuralgia / Q000378:metabolism*; D010147:Pain Measurement; D011930:Reaction Time
C498197:Cacna1g protein, mouse; D020747:Calcium Channels, T-Type