Journal
PAIN
Volume 96, Issue 3, Pages 269-277Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1016/S0304-3959(01)00456-0
Keywords
voltage-gated sodium channel; Na(v)1.8; Na(v)1.9; pain; neuropathic pain; nerve injury; dorsal root ganglia
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Funding
- NINDS NIH HHS [1 R01 NS39518, 5 R01 NS38253-03] Funding Source: Medline
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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, Na(v)1.8 (SNS/PN3) and Na(v)1.9 (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 Na(v)1.8 and Na(v)1.9 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 Na(v)1.8 and Na(v)1.9 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. (C) 2002 International Association for the Study of Pain. Published by Elsevier Science B.V. All rights reserved.
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