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Papers of the Week

Papers: 23 Feb 2019 - 1 Mar 2019

Animal Studies

2019 Jan-Dec

Mol Pain


Nerve injury elevates functional Cav3.2 channels in superficial spinal dorsal horn.


Feng X-J, Ma L-X, Jiao C, Kuang H-X, Zeng F, Zhou X-Y, Cheng X-E, Zhu M-Y, Zhang D-Y, Jiang C-Y, Liu T
Mol Pain. 2019 Jan-Dec; 15:1744806919836569.
PMID: 30803310.


Cav3 channels play an important role in modulating chronic pain. However, less is known about the functional changes of Cav3 channels in superficial spinal dorsal horn (SDH) in neuropathic pain states. Here, we examined the effect of partial sciatic nerve ligation (PSNL) on either expression or electrophysiological properties of Cav3 channels in superficial SDH. Our in vivo studies showed that the blockers of Cav3 channels robustly alleviated PSNL-induced mechanical allodynia and thermal hyperalgesia, which lasted at least 14 days following PSNL. Meanwhile, PSNL triggered an increase in both mRNA and protein levels of Cav3.2, but not Cav3.1 or Cav3.3 in rats. However, in Cav3.2 knockout (KO) mice, PSNL predominantly attenuated mechanical allodynia but not thermal hyperalgesia. In addition, the results of whole-cell patch-clamp recordings showed that both the overall proportion of Cav3 current-expressing neurons and the Cav3 current density in individual neurons were elevated in spinal lamina II neurons from PSNL rats, which could not be recapitulated in Cav3.2 KO mice. Altogether, our findings reveal that the elevated functional Cav3.2 channels in superficial SDH may contribute to the mechanical allodynia in PSNL-induced neuropathic pain model.