Related resources
Search for item elsewhere
University researcher(s)
Academic department(s)
Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger
Shembalkar P. K, Till S, Boettger M. K, Terenghi G, Tate S, Bountra C, Anand P
Eur J Pain. 2001;5, 3:319-23.
Access to files
Full-text and supplementary files are not available from Manchester eScholar. Use our list of Related resources to find this item elsewhere. Alternatively, request a copy from the Library's Document supply service.
Abstract
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.
Keyword(s)
*Nerve Growth Factors; Aged; Amputation Stumps/pathology/physiopathology; Causalgia/*metabolism/physiopathology; Female; Fingers/innervation/*physiopathology/surgery; Human; Immunohistochemistry; Mechanoreceptors/metabolism/pathology; Nerve Fibers/metabolism/pathology; Nerve Tissue Proteins/*deficiency; Neurons, Afferent/*metabolism; Neuropeptides/*metabolism; Nociceptors/*metabolism/physiopathology; Postoperative Complications/metabolism/physiopathology; Radial Nerve/*metabolism/physiopathology; Sodium Channels/*metabolism
Bibliographic metadata
- 1090-3801Case ReportsJournal Article