Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger

The sodium channels SNS/PN3 and NaN/SNS2 are regulated by the neurotrophic factors-nerve growth factor (NGF) and glial-derived neurotrophic factor (GD NF), and may play an important role in the development of pain after nerve injury or inflammation. These key molecules have been studied in an amputat ed causalgic finger and control tissues by immunohistochemistry. There was a marked increase in the number and intensity of SNS/PN3-immunoreactive ner ve terminals in the affected finger, while GDNF-immunoreactivity was not ob served, in contrast to controls. No differences were observed for NGF, trk A, NT-3 or NaN/SNS2-immunoreactivity. While further studies are required, t hese findings suggest that accumulation of SNS/PN3 and/or loss of GDNF may contribute to pain in causalgia, and that selective blockers of SNS/PN3 and /or rhGDNF may provide effective novel treatments. (C) 2001 European Federa tion of Chapters of the International Association for the study of Pain.