The pattern of expression of the voltage-gated sodium channels Na(v)1.8 and Na(v)1.9 does not change in uninjured primary sensory neurons in experimental neuropathic pain models

Details

Serval ID
serval:BIB_438B686B8F7A
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
The pattern of expression of the voltage-gated sodium channels Na(v)1.8 and Na(v)1.9 does not change in uninjured primary sensory neurons in experimental neuropathic pain models
Journal
Pain
Author(s)
Decosterd  I., Ji  R. R., Abdi  S., Tate  S., Woolf  C. J.
ISSN
0304-3959 (Print)
Publication state
Published
Issued date
04/2002
Volume
96
Number
3
Pages
269-77
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Apr
Abstract
A spared nerve injury of the sciatic nerve (SNI) or a segmental lesion of the L5 and L6 spinal nerves (SNL) lead to behavioral signs of neuropathic pain in the territory innervated by adjacent uninjured nerve fibers, while a chronic constriction injury (CCI) results in pain sensitivity in the affected area. While alterations in voltage-gated sodium channels (VGSCs) have been shown to contribute to the generation of ectopic activity in the injured neurons, little is known about changes in VGSCs in the neighboring intact dorsal root ganglion (DRG) neurons, even though these cells begin to fire spontaneously. We have now investigated changes in the expression of the TTX-resistant VGSCs, Nav1.8 (SNS/PN3) and Nav1.9 (SNS2/NaN) by immunohistochemistry in rat models of neuropathic pain both with an intermingling of intact and degenerated axons in the nerve stump (SNL and CCI) and with a co-mingling in the same DRG of neurons with injured and uninjured axons (sciatic axotomy and SNI). The expression of Nav1.8 and Nav1.9 protein was abolished in all injured DRG neurons, in all models. In intact DRGs and in neighboring non-injured neurons, the expression and the distribution among the A- and C-fiber neuronal populations of Nav1.8 and Nav1.9 was, however, unchanged. While it is unlikely, therefore, that a change in the expression of TTX-resistant VGSCs in non-injured neurons contributes to neuropathic pain, it is essential that molecular alterations in both injured and non-injured neurons in neuropathic pain models are investigated.
Keywords
Animals Axotomy Cell Size Ganglia, Spinal/*cytology Male Neurons, Afferent/cytology/*metabolism Neuropeptides/analysis/*biosynthesis Rats Rats, Sprague-Dawley Sciatic Nerve/injuries/metabolism Sciatica/*metabolism Sodium Channels/analysis/*biosynthesis Spinal Nerve Roots/injuries/metabolism Sural Nerve/metabolism
Pubmed
Web of science
Create date
28/01/2008 10:45
Last modification date
20/08/2019 13:47
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