Nociceptor-specific gene deletion using heterozygous NaV1. 8-Cre recombinase mice

CL Stirling, G Forlani, MD Baker, JN Wood… - Pain, 2005 - journals.lww.com
CL Stirling, G Forlani, MD Baker, JN Wood, EA Matthews, AH Dickenson, MA Nassar
Pain, 2005journals.lww.com
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 …
Abstract
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.
Lippincott Williams & Wilkins