Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain

Citation
Sd. Dib-hajj et al., Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain, PAIN, 83(3), 1999, pp. 591-600
Citations number
56
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
PAIN
ISSN journal
03043959 → ACNP
Volume
83
Issue
3
Year of publication
1999
Pages
591 - 600
Database
ISI
SICI code
0304-3959(199912)83:3<591:POSCEI>2.0.ZU;2-9
Abstract
Previous studies have shown that transection of the sciatic nerve induces d ramatic changes in sodium currents of axotomized dorsal root ganglion (DRG) neurons, which are paralleled by significant changes in the levels of tran scripts of several sodium channels expressed in these neurons. Sodium curre nts that are resistant to tetrodotoxin (TTX-R) and the transcripts of two T TX-R sodium channels are significantly attenuated, while a rapidly reprimin g tetrodotoxin-sensitive (TTX-S) current emerges and the transcripts of alp ha-III sodium channel, which produce a TTX-S current when expressed in oocy tes, are up-regulated. We report here on changes in sodium currents and sod ium channel transcripts in DRG neurons in the chronic constriction injury ( CCI) model of neuropathic pain. CCI-induced changes in DRG neurons, 14 days post-surgery, mirror those of axotomy. Transcripts of NaN and SNS, two sen sory neuron-specific TTX-R sodium channels, are significantly down-regulate d as is the TTX-R sodium current, while transcripts of the TTX-S alpha-III sodium channel and a rapidly repriming TTX-S Na current are up-regulated in small diameter DRG neurons. These changes may provide at least a partial b asis for the hyperexcitablity of DRG neurons that contributes to hyperalges ia in this model. (C) 1999 International Association for the Study of Pain. Published by Elsevier Science B.V.