Autotomy behavior correlates with the DRG and spinal expression of sodium channels in inbred mouse strains

Anna Karin Persson*, Jonas Thun, Xiao Jun Xu, Zsuzsanna Wiesenfeld-Hallin, Mikael Ström, Marshall Devor, Olle Lidman, Kaj Fried

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Patients who have suffered nerve injury show profound inter-individual variability in neuropathic pain even when the precipitating injury is nearly identical. Variability in pain behavior is also observed across inbred strains of mice where it has been attributed to genetic polymorphisms. Identification of cellular correlates of pain variability across strains can advance the understanding of underlying pain mechanisms. Voltage-gated sodium channels (VGSCs) play a major role in the generation and propagation of action potentials in the primary afferents and are therefore of obvious importance for pain phenotype. Here, we examined the mRNA expression levels of the VGSC α-subunits Nav1.3, Nav1.5, Nav1.6, and Nav1.7, as well as the auxiliary VGSC-related molecule, Contactin. Dorsal root ganglia (DRG) and spinal cords from 5 inbred mouse strains with contrasting pain phenotype (AKR/J, C3H/HeJ, C57BL/6J, C58/J and CBA/J) were analyzed 7 days following sciatic and saphenous nerve transection. In the DRG, Nav1.6, Nav1.7 and Contactin were abundantly expressed in control animals. Following nerve injury, the residual mRNA levels of Nav1.6 (downregulated in two of the strains) correlated tightly to the extent of autotomy behavior. A suggestive correlation was also seen for the post-injury mRNA levels of Contactin (downregulated in all strains) with autotomy. Thus, our results suggest a contribution by DRG Nav1.6, and possibly Contactin to neuropathic pain in the neuroma model in mice.

Original languageEnglish
Pages (from-to)1-13
Number of pages13
JournalBrain Research
Volume1285
DOIs
StatePublished - 18 Aug 2009

Keywords

  • Dorsal root ganglion
  • Gene regulation
  • Neuropathic pain
  • Pain genetics
  • Sciatic nerve
  • Voltage-gated sodium channels

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