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The sodium channels SNS/PN3 and NaN/SNS2 are regulated by the neurotrophic factors-nerve growth factor (NGF) and glial-derived neurotrophic factor (GDNF), and may play an important role in the development of pain after nerve injury or inflammation. These key molecules have been studied in an amputated causalgic finger and control tissues by immunohistochemistry. There was a marked increase in the number and intensity of SNS/PN3-immunoreactive nerve terminals in the affected finger, while GDNF-immunoreactivity was not observed, in contrast to controls. No differences were observed for NGF, trk A, NT-3 or NaN/SNS2-immunoreactivity. While further studies are required, these 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.

Original publication

DOI

10.1053/eujp.2001.0251

Type

Journal article

Journal

Eur J Pain

Publication Date

2001

Volume

5

Pages

319 - 323

Keywords

Aged, Amputation Stumps, Causalgia, Female, Fingers, Glial Cell Line-Derived Neurotrophic Factor, Humans, Immunohistochemistry, Mechanoreceptors, NAV1.8 Voltage-Gated Sodium Channel, Nerve Fibers, Nerve Growth Factors, Nerve Tissue Proteins, Neurons, Afferent, Neuropeptides, Nociceptors, Postoperative Complications, Radial Nerve, Sodium Channels