The molecular basis of analgesia in congenital insensitivity to pain associated with loss of Nav1.7 function

ABSTRACT: Loss of function mutations in the SCN9a gene encoding voltage-gated sodium channel Nav1.7 cause congenital insensitivity to pain (CIP) and anosmia in otherwise normal humans and mice, suggesting that this channel may be a good analgesic drug target. Surprisingly, potent selective antagonists of Nav1.7 are weak analgesics. We therefore investigated whether Nav1.7 , as well as contributing to electrical signalling may have an additional function. Here we report that Nav1.7 deletion has profound effects on the sensory neuron transcriptome, leading to dysregulation of a number of transcription factors as well as upregulation of enkephalin precursor PENK mRNA and down regulation of CEACAM10 mRNA, a protein involved in noxious thermosensation. PENK mRNA is transcriptionally upregulated

ORGANISM(S): Mus musculus

SUBMITTER: John Wood 

PROVIDER: E-GEOD-61373 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress