Mice congenic for a locus that determines phenotype in the neuroma model of neuropathic pain.

Abstract

A common strategy for identifying physiological processes responsible for pain is to compare animal strains that show high versus low pain phenotype. However, this approach yields only weak inference because most strains differ from one another at a large number of genetic loci. We undertook a congenic breeding program aimed at transposing the gene(s) that confers dominant (low) pain phenotype in the neuroma model of neuropathic pain from mice of the C58/J strain onto a genetic background that normally expresses high pain phenotype (C3H/HeN). Successful transposition, and the observation of equal numbers of phenotypically high and low offspring in each of 11 generations of selective breeding, provides evidence that the trait is largely controlled by a single gene (or linked cluster) of major effect.