Positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury

  • Authors:
    • Guixia Li
    • Xifang Liu
    • Jingnan Du
    • Jianzhao Chen
    • Fenglin She
    • Chunfu Wu
    • Chunli Li
  • View Affiliations

  • Published online on: May 25, 2015     https://doi.org/10.3892/mmr.2015.3839
  • Pages: 3583-3590
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Neuropathic pain is a global medical concern, characterized by spontaneous pain, heat hyperalgesia and mechanical allodynia. The condition has been associated with alterations in the voltage‑gated sodium channels, Nav1.8 and Nav1.9, in nociceptive neurons termed nociceptors. However, an explanation for the contribution of these channels to the phenotype observed in neuropathic pain remains to be elucidated. The changes induced by chronic constriction injury (CCI) to Nav1.8 and Nav1.9 mRNA and protein levels, as well as electrical currents in injured and contralateral non‑injured dorsal root ganglion (DRG) neurons are described in the present study. A marked downregulation was observed for each Nav isoform transcript and protein expressed in injured neurons with the exception of the Nav1.9 protein, which exhibited no change, while in contralateral non‑injured neurons, the levels of protein and mRNA remained unchanged. Nav isoform functional analysis was then performed in L4‑6 DRG neurons 14 days after CCI. The Nav1.8 current density was markedly decreased in injured DRG neurons following CCI. The voltage‑dependent activation of the Nav1.8 channel in these neurons was shifted to depolarized potentials by 5.3 mV, while it was shifted to hyperpolarized potentials by 10 mV for inactivation. The electrophysiological function of Nav1.9 was not affected by CCI. The present study demonstrated that ectopic discharge following CCI, which was likely induced by a positive shift in the Nav1.8 current inactivation curve in injured neurons, enhanced the excitability of the neurons by facilitating tetrodotoxin‑resistant sodium channels into the fast inactivation state and did not occur as a result of a compensatory redistribution in the contralateral uninjured neurons.
View Figures
View References

Related Articles

Journal Cover

September-2015
Volume 12 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Li G, Liu X, Du J, Chen J, She F, Wu C and Li C: Positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury. Mol Med Rep 12: 3583-3590, 2015.
APA
Li, G., Liu, X., Du, J., Chen, J., She, F., Wu, C., & Li, C. (2015). Positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury. Molecular Medicine Reports, 12, 3583-3590. https://doi.org/10.3892/mmr.2015.3839
MLA
Li, G., Liu, X., Du, J., Chen, J., She, F., Wu, C., Li, C."Positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury". Molecular Medicine Reports 12.3 (2015): 3583-3590.
Chicago
Li, G., Liu, X., Du, J., Chen, J., She, F., Wu, C., Li, C."Positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury". Molecular Medicine Reports 12, no. 3 (2015): 3583-3590. https://doi.org/10.3892/mmr.2015.3839