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
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.