Nav1.9 Channel Contributes to Mechanical and Heat Pain Hypersensitivity Induced by Subacute and Chronic Inflammation
2011

Nav1.9 Channel and Inflammatory Pain

Sample size: 9 publication 10 minutes Evidence: high

Author Information

Author(s): Lolignier Stéphane, Amsalem Muriel, Maingret François, Padilla Françoise, Gabriac Mélanie, Chapuy Eric, Eschalier Alain, Delmas Patrick, Busserolles Jérôme

Primary Institution: Clermont Université, Laboratoire de Pharmacologie Fondamentale et Clinique de la Douleur, Clermont-Ferrand, France

Hypothesis

Does the Nav1.9 channel contribute to mechanical and heat pain hypersensitivity induced by inflammation?

Conclusion

The Nav1.9 channel plays a crucial role in the generation of heat and mechanical pain hypersensitivity during both subacute and chronic inflammatory pain models.

Supporting Evidence

  • Nav1.9-null mice showed reduced heat and mechanical pain hypersensitivity in response to inflammation.
  • Behavioral results were correlated with molecular and electrophysiological analyses.
  • Nav1.9 channel expression was found to be modulated during inflammation.

Takeaway

The Nav1.9 channel helps our body feel pain when we have inflammation, like when we hurt our ankle or get a sore paw.

Methodology

The study used Nav1.9-null mice and Nav1.9 knock-down rats to assess pain hypersensitivity through various behavioral tests.

Limitations

The study may not generalize to all inflammatory pain models, as discrepancies exist between different models.

Participant Demographics

Mice and rats used in the study were of specific strains (C57Bl6/J and Sprague Dawley) and ages (8-14 weeks for mice, 150-175 g for rats).

Statistical Information

P-Value

p≤0.003

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0023083

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