• Mol. Cell. Neurosci. · Feb 2008

    Transcriptional and functional profiles of voltage-gated Na(+) channels in injured and non-injured DRG neurons in the SNI model of neuropathic pain.

    • Temugin Berta, Olivier Poirot, Marie Pertin, Ru-Rong Ji, Stephan Kellenberger, and Isabelle Decosterd.
    • Department of Anesthesiology, University Hospital Center and University of Lausanne, CH-1011 Lausanne, Switzerland. temugin.berta@unil.ch
    • Mol. Cell. Neurosci. 2008 Feb 1;37(2):196-208.

    AbstractChanges in expression and function of voltage-gated sodium channels (VGSC) in dorsal root ganglion (DRG) neurons may play a major role in the genesis of peripheral hyperexcitability that occurs in neuropathic pain. We present here the first description of changes induced by spared nerve injury (SNI) to Na(v)1 mRNA levels and tetrodotoxin-sensitive and -resistant (TTX-S/TTX-R) Na(+) currents in injured and adjacent non-injured small DRG neurons. VGSC transcripts were down-regulated in injured neurons except for Na(v)1.3, which increased, while they were either unchanged or increased in non-injured neurons. TTX-R current densities were reduced in injured neurons and the voltage dependence of steady-state inactivation for TTX-R was positively shifted in injured and non-injured neurons. TTX-S current densities were not affected by SNI, while the rate of recovery from inactivation was accelerated in injured neurons. Our results describe altered neuronal electrogenesis following SNI that is likely induced by a complex regulation of VGSCs.

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