| First Author | Stirling LC | Year | 2005 |
| Journal | Pain | Volume | 113 |
| Issue | 1-2 | Pages | 27-36 |
| PubMed ID | 15621361 | Mgi Jnum | J:99609 |
| Mgi Id | MGI:3583070 | Doi | 10.1016/j.pain.2004.08.015 |
| Citation | Stirling LC, et al. (2005) Nociceptor-specific gene deletion using heterozygous NaV1.8-Cre recombinase mice. Pain 113(1-2):27-36 |
| abstractText | NaV1.8 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 NaV1.8 promoter. Functional Cre recombinase expression replicated precisely the expression pattern of NaV1.8. 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 NaV1.8-Cre mouse line is a useful tool to analyse the effects of deleting floxed genes on pain behaviour. |
