4.6 Article

Nociceptor-specific gene deletion using heterozygous Na(v)1.8-Cre recombinase mice

Journal

PAIN
Volume 113, Issue 1-2, Pages 27-36

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.pain.2004.08.015

Keywords

pain; knock-out; Cre-loxP; sodium channel; behaviour

Funding

  1. Medical Research Council [G9717869] Funding Source: Medline
  2. MRC [G9717869] Funding Source: UKRI

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Na(v)1.8 is a voltage-gated sodium channel expressed only in a subset of sensory neurons of which more than 85% are nociceptors. In order to delete genes in nociceptive neurons, we generated heterozygous transgenic mice expressing Cre recombinase under the control of the Na(v)1.8 promoter. Functional Cre recombinase expression replicated precisely the expression pattern of Na(v)1.8. Cre expression began at embryonic day 14 in small diameter neurons in dorsal root, trigeminal and nodose ganglia, but was absent in non-neuronal or CNS tissues into adulthood. Sodium channel subtypes were normal in isolated DRG neurons. Pain behaviour in response to mechanical or thermal stimuli, and in acute, inflammatory and neuropathic pain was also normal. These data demonstrate that the heterozygous Na(v)1.8-Cre mouse line is a useful tool to analyse the effects of deleting floxed genes on pain behaviour. (C) 2004 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

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