Blockade of Persistent Sodium Currents Contributes to the Riluzole-Induced Inhibition of Spontaneous Activity and Oscillations in Injured DRG Neurons
2011

Riluzole Reduces Pain Signals in Injured Nerve Cells

Sample size: 53 publication 10 minutes Evidence: moderate

Author Information

Author(s): Xie Rou-Gang, Zheng Da-Wei, Xing Jun-Ling, Zhang Xu-Jie, Song Ying, Xie Ya-Bin, Kuang Fang, Dong Hui, You Si-Wei, Xu Hui, Hu San-Jue

Primary Institution: Institute of Neuroscience, Xi Jing Hospital, The Fourth Military Medical University, Xi'an, People's Republic of China

Hypothesis

The study investigates whether the INaP blocker riluzole can inhibit spontaneous activity in injured DRG neurons.

Conclusion

Riluzole effectively inhibits the persistent sodium current in injured DRG neurons, suggesting it may be a potential treatment for neuropathic pain.

Supporting Evidence

  • Riluzole significantly inhibited the spontaneous activity of A-type DRG neurons in a dose-dependent manner.
  • The INaP was enhanced in medium- and large-sized neurons of the compressed DRG.
  • Local application of riluzole abolished subthreshold membrane potential oscillations in DRG neurons.
  • Behavioral tests showed that CCD rats developed mechanical allodynia, which was correlated with increased INaP.

Takeaway

Riluzole is a medicine that can help reduce pain signals in injured nerve cells, making it easier for people to feel better.

Methodology

The study used in vivo recordings from rat DRG neurons to assess the effects of riluzole on spontaneous activity and membrane potential oscillations.

Limitations

The study primarily focused on a specific animal model and may not fully translate to human conditions.

Participant Demographics

Adult Sprague-Dawley rats of both sexes, weighing 200-250 g.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0018681

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication