Research

Nerve injury induces robust allodynia and ectopic discharges in Na_v1.3 null mutant mice

Mohammed A Nassar¹ , Mark D Baker¹ , Alessandra Levato¹ , Rachel Ingram² , Giovanna Mallucci³ , Stephen B McMahon² and John N Wood¹

¹  Molecular Nociception Group, Department of Biology, University College London WC1E 6BT, UK

²  Centre for Neuroscience Research, Kings College London, London SE1 7EH, UK

³  MRC Prion Unit and Department of Neurodegeneration. Institute of Neurology, Queen Square, London WC1N 3BG, UK

author email corresponding author email

Molecular Pain 2006, 2:33doi:10.1186/1744-8069-2-33

Published:	19 October 2006

Abstract

Changes in sodium channel activity and neuronal hyperexcitability contribute to neuropathic pain, a major clinical problem. There is strong evidence that the re-expression of the embryonic voltage-gated sodium channel subunit Na_v1.3 underlies neuronal hyperexcitability and neuropathic pain.

Here we show that acute and inflammatory pain behaviour is unchanged in global Na_v1.3 mutant mice. Surprisingly, neuropathic pain also developed normally in the Na_v1.3 mutant mouse. To rule out any genetic compensation mechanisms that may have masked the phenotype, we investigated neuropathic pain in two conditional Na_v1.3 mutant mouse lines. We used Na_v1.8-Cre mice to delete Nav1.3 in nociceptors at E14 and NFH-Cre mice to delete Na_v1.3 throughout the nervous system postnatally. Again normal levels of neuropathic pain developed after nerve injury in both lines. Furthermore, ectopic discharges from damaged nerves were unaffected by the absence of Na_v1.3 in global knock-out mice. Our data demonstrate that Na_v1.3 is neither necessary nor sufficient for the development of nerve-injury related pain.