Wednesday, December 20, 2006

Abolishing pain with a single sodium channel mutation

Even though this blog is mainly about nervous systems, brains, and behaviors, I'm occasionally drawn back to my roots as a molecular biologist by a particularly outstanding example of how a single molecule can determine what we take to be a very complex experience - in this case the experience of pain. Cox et. al. have found that a mutation in the gene for a particular sodium channel subunit that is strongly expressed in the pain sensitivie endings of nociceptive (pain sensing and transmitting) neurons can abolish the ability to feel pain. The rare mutation was found in several individuals from a family in northern Pakistan who were unable to experience pain. This work should stimulate the search for novel analgesics that selectively target this sodium channel subunit.

The ususual human situation that permitted this work is described: "The index case for the present study was a ten-year-old child, well known to the medical service after regularly performing 'street theatre'. He placed knives through his arms and walked on burning coals, but experienced no pain. He died before being seen on his fourteenth birthday, after jumping off a house roof. Subsequently, we studied three further consanguineous families in which there were individuals with similar histories of a lack of pain appreciation, each originating from northern Pakistan and part of the Qureshi birdari/clan. All six affected individuals had never felt any pain, at any time, in any part of their body...All had injuries to their lips (some requiring later plastic surgery) and/or tongue (with loss of the distal third in two cases), caused by biting themselves in the first 4 yr of life. All had frequent bruises and cuts, and most had suffered fractures or osteomyelitis, which were only diagnosed in retrospect because of painless limping or lack of use of a limb. The children were considered of normal intelligence by their parents and teachers, and by the caring physicians."

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