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 (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 amputat...
| Päätekijät: | , , , , , , |
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| Aineistotyyppi: | Journal article |
| Kieli: | English |
| Julkaistu: |
2001
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| _version_ | 1826295000659394560 |
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| author | Shembalkar, P Till, S Boettger, M Terenghi, G Tate, S Bountra, C Anand, P |
| author_facet | Shembalkar, P Till, S Boettger, M Terenghi, G Tate, S Bountra, C Anand, P |
| author_sort | Shembalkar, P |
| collection | OXFORD |
| description | 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. |
| first_indexed | 2024-03-07T03:54:22Z |
| format | Journal article |
| id | oxford-uuid:c25b38ac-e369-4240-b627-7f20433855f0 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T03:54:22Z |
| publishDate | 2001 |
| record_format | dspace |
| spelling | oxford-uuid:c25b38ac-e369-4240-b627-7f20433855f02022-03-27T06:08:27ZIncreased sodium channel SNS/PN3 immunoreactivity in a causalgic finger.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:c25b38ac-e369-4240-b627-7f20433855f0EnglishSymplectic Elements at Oxford2001Shembalkar, PTill, SBoettger, MTerenghi, GTate, SBountra, CAnand, PThe 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. |
| spellingShingle | Shembalkar, P Till, S Boettger, M Terenghi, G Tate, S Bountra, C Anand, P Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger. |
| title | Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger. |
| title_full | Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger. |
| title_fullStr | Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger. |
| title_full_unstemmed | Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger. |
| title_short | Increased sodium channel SNS/PN3 immunoreactivity in a causalgic finger. |
| title_sort | increased sodium channel sns pn3 immunoreactivity in a causalgic finger |
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