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Attenuated Neuropathic Pain in CaV3.1 Null Mice  

Na, Heung Sik (Department of Physiology, Korea University College of Medicine)
Choi, Soonwook (Center for Neural Science, Korea Institute of Science and Technology)
Kim, Junesun (Department of Physiology, Korea University College of Medicine)
Park, Joonoh (Center for Neural Science, Korea Institute of Science and Technology)
Shin, Hee-Sup (Center for Neural Science, Korea Institute of Science and Technology)
Abstract
To assess the role of $\alpha_{1G}$ T-type $Ca^{2+}$ channels in neuropathic pain after L5 spinal nerve ligation, we examined behavioral pain susceptibility in mice lacking $Ca_{V}3.1$ (${\alpha}_{1G}{^{-/-}}$), 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 ${{\alpha}_{1G}}^{-/-}$ 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 $Ca^{2+}$ channels in the development of neuropathic pain, and suggest that selective modulation of ${\alpha}_{1G}$ subtype channels may provide a novel approach to the treatment of allodynia and hyperalgesia.
Keywords
Allodynia; Central Sensitization; Hyperalgesia; Spinal Nerve Ligation (SNL); T-Type Calcium Channel;
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