Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger

P. K. Shembalkar; S. Till; M. K. Boettger; G. Terenghi; S. Tate; C. Bountra; P. Anand

doi:10.1053/eujp.2001.0251

Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger

P. K. Shembalkar, S. Till, M. K. Boettger, G. Terenghi, S. Tate, C. Bountra, P. Anand

Research output: Contribution to journal › Article › peer-review

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. © 2001 European Federation of Chapters of the International Association for the study of Pain.

Original language	English
Pages (from-to)	319-323
Number of pages	4
Journal	European Journal of Pain
Volume	5
Issue number	3
DOIs	https://doi.org/10.1053/eujp.2001.0251
Publication status	Published - 2001

Keywords

Causalgia
GDNF
Pain
SNS/PN3
Sodium channels

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10.1053/eujp.2001.0251

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title = "Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger",

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. {\textcopyright} 2001 European Federation of Chapters of the International Association for the study of Pain.",

keywords = "Causalgia, GDNF, Pain, SNS/PN3, Sodium channels",

author = "Shembalkar, {P. K.} and S. Till and Boettger, {M. K.} and G. Terenghi and S. Tate and C. Bountra and P. Anand",

year = "2001",

doi = "10.1053/eujp.2001.0251",

language = "English",

volume = "5",

pages = "319--323",

journal = "European Journal of Pain",

issn = "1090-3801",

publisher = "John Wiley & Sons Ltd",

number = "3",

}

TY - JOUR

T1 - Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger

AU - Shembalkar, P. K.

AU - Till, S.

AU - Boettger, M. K.

AU - Terenghi, G.

AU - Tate, S.

AU - Bountra, C.

AU - Anand, P.

PY - 2001

Y1 - 2001

N2 - 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. © 2001 European Federation of Chapters of the International Association for the study of Pain.

AB - 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. © 2001 European Federation of Chapters of the International Association for the study of Pain.

KW - Causalgia

KW - GDNF

KW - Pain

KW - SNS/PN3

KW - Sodium channels

U2 - 10.1053/eujp.2001.0251

DO - 10.1053/eujp.2001.0251

M3 - Article

SN - 1090-3801

VL - 5

SP - 319

EP - 323

JO - European Journal of Pain

JF - European Journal of Pain

IS - 3

ER -

Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger

Abstract

Keywords

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