title: Nociceptor-specific gene deletion using heterozygous NaV1.8-Cre recombinase mice.
abstract: 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.
authors.affiliation: Molecular Nociception Group, Biology Department, University College London, Gower Street, London WC1E 6BT, UK.
authors.forename: L Caroline
authors.initials: LC
authors.lastname: Stirling
authors.forename: Greta
authors.initials: G
authors.lastname: Forlani
authors.forename: Mark D
authors.initials: MD
authors.lastname: Baker
authors.forename: John N
authors.initials: JN
authors.lastname: Wood
authors.forename: Elizabeth A
authors.initials: EA
authors.lastname: Matthews
authors.forename: Anthony H
authors.initials: AH
authors.lastname: Dickenson
authors.forename: Mohammed A
authors.initials: MA
authors.lastname: Nassar
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D004622:Embryo, Mammalian; D005260:Female; D005727:Ganglia, Spinal / Q000166:cytology; D017353:Gene Deletion; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology; D006579:Heterozygote; D007150:Immunohistochemistry / Q000379:methods; D019426:Integrases / Q000235:genetics / Q000378:metabolism*; D007381:Intermediate Filament Proteins / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D008822:Mice, Transgenic; D009043:Motor Activity / Q000502:physiology; D062559:NAV1.8 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins / Q000378:metabolism; D016900:Neurofilament Proteins / Q000378:metabolism; D009474:Neurons / Q000502:physiology; D009619:Nociceptors / Q000378:metabolism*; D010146:Pain / Q000503:physiopathology; D010147:Pain Measurement / Q000379:methods; D017288:Pain Threshold / Q000502:physiology; D018408:Patch-Clamp Techniques / Q000379:methods; D064531:Peripherins; D010812:Physical Stimulation / Q000379:methods; D011597:Psychomotor Performance / Q000502:physiology; D011930:Reaction Time / Q000502:physiology; D045442:Rotarod Performance Test / Q000379:methods; D020426:Sciatic Neuropathy / Q000503:physiopathology; D015222:Sodium Channels / Q000235:genetics / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors; D014599:Uterus / Q000378:metabolism; D001616:beta-Galactosidase / Q000378:metabolism
chemical_list: D007381:Intermediate Filament Proteins; D008562:Membrane Glycoproteins; D062559:NAV1.8 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins; D016900:Neurofilament Proteins; D064531:Peripherins; C568318:Scn10a protein, mouse; D015222:Sodium Channels; C051774:neurofilament protein H; D013779:Tetrodotoxin; C045073:Cre recombinase; D019426:Integrases; D001616:beta-Galactosidase