Mutations in ion channel prevent pain

New analgesics could result from the recent identification of mutations that block a pain pathway. University of Cambridge medical geneticist C. Geoffrey Woods and colleagues studied members of three Pakistani families who are unable to feel pain. That inability may sound like a blessing, but pain is a useful signal to modify harmful behavior. Each of the members of the study group had suffered injuries, including fractures or bone infections that were "only diagnosed in retrospect because of painless limping or lack of use of a limb," the researchers report. They traced the Pakistanis' rare condition to mutations in the SCN9A gene (Nature 2006, 444, 894). The gene codes for Na_v1.7, a subunit of a voltage-gated sodium channel that is abundant in pain-signaling neurons. Because the mutations produce nonfunctional Na_v1.7, the researchers conclude that SCN9A is essential for feeling pain. They hope their findings will prompt a search for analgesics to target this sodium channel subunit in people without the Na_v1.7 mutations.