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The Journal of Neurophysiology Vol. 82 No. 5 November 1999, pp. 2776-2785
Copyright ©1999 by the American Physiological Society
1Department of Neurology and 2Paralyzed Veterans of America/Eastern Paralyzed Veterans Association Center for Neuroscience Research, Yale University School of Medicine, New Haven, Connecticut 06520; 3Rehabilitation Research Center, Veterans Affairs Connecticut, West Haven, Connecticut 06516; and 4Molecular Pharmacology Unit, Glaxo-Wellcome Research and Development, Medicines Research Centre, Stevenage, Hertfordshire SG1 2NY, United Kingdom
Black, J. A.,
T. R. Cummins,
C. Plumpton,
Y. H. Chen,
W. Hormuzdiar,
J. J. Clare, and
S. G. Waxman.
Upregulation of a Silent Sodium Channel After Peripheral, but not
Central, Nerve Injury in DRG Neurons. J. Neurophysiol. 82: 2776-2785, 1999. After transection of
their axons within the sciatic nerve, DRG neurons become
hyperexcitable. Recent studies have demonstrated the emergence of a
rapidly repriming tetrodotoxin (TTX)-sensitive sodium current that may
account for this hyperexcitability in axotomized small (<27 µm diam)
DRG neurons, but its molecular basis has remained unexplained. It has
been shown previously that sciatic nerve transection leads to an
upregulation of sodium channel III transcripts, which normally are
present at very low levels in DRG neurons, in adult rats. We show here
that TTX-sensitive currents in small DRG neurons, after transection of
their peripheral axonal projections, reprime more rapidly than those in
control neurons throughout a voltage range of 
140 to 60 mV, a
finding that suggests that these currents are produced by a different sodium channel. After transection of the central axonal projections (dorsal rhizotomy) of these small DRG neurons, in contrast, the repriming kinetics of TTX-sensitive sodium currents remain similar to
those of control (uninjured) neurons. We also demonstrate, with two
distinct antibodies directed against different regions of the type III
sodium channel, that small DRG neurons display increased brain type III
immunostaining when studied 7-12 days after transection of their
peripheral, but not central, projections. Type III sodium channel
immunoreactivity is present within somata and neurites of peripherally
axotomized, but not centrally axotomized, neurons studied after <24 h
in vitro. Peripherally axotomized DRG neurons in situ also exhibit
enhanced type III staining compared with control neurons, including an
accumulation of type III sodium channels in the distal portion of the
ligated and transected sciatic nerve, but these changes are not seen in
centrally axotomized neurons. These observations are consistent with a
contribution of type III sodium channels to the rapidly repriming
sodium currents observed in peripherally axotomized DRG neurons and
suggest that type III channels may at least partially account for the
hyperexcitibility of these neurons after injury.
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