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The Journal of Neurophysiology Vol. 86 No. 2 August 2001, pp. 629-640
Copyright ©2001 by the American Physiological Society
Department of Neurology and Paralyzed Veterans of America/Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven 06510; and Rehabilitation Research Center, Veterans Affairs Connecticut Healthcare Center, West Haven, Connecticut 06516
Renganathan, Muthukrishnan,
Theodore R. Cummins, and
Stephen G. Waxman.
Contribution of Nav1.8 Sodium Channels to
Action Potential Electrogenesis in DRG Neurons. J. Neurophysiol. 86: 629-640, 2001. C-type dorsal root
ganglion (DRG) neurons can generate tetrodotoxin-resistant (TTX-R)
sodium-dependent action potentials. However, multiple sodium channels
are expressed in these neurons, and the molecular identity of the TTX-R
sodium channels that contribute to action potential production in these
neurons has not been established. In this study, we used current-clamp
recordings to compare action potential electrogenesis in
Nav1.8 (+/+) and (
/) small DRG neurons maintained for 2-8 h in vitro to examine the role of sodium channel Nav1.8 (
-SNS) in action potential
electrogenesis. Although there was no significant difference in resting
membrane potential, input resistance, current threshold, or voltage
threshold in Nav1.8 (+/+) and (/) DRG
neurons, there were significant differences in action potential
electrogenesis. Most Nav1.8 (+/+) neurons generate all-or-none action potentials, whereas most of
Nav1.8 (/) neurons produce smaller graded
responses. The peak of the response was significantly reduced in
Nav1.8 (/) neurons [31.5 ± 2.2 (SE) mV] compared with Nav1.8 (+/+)
neurons (55.0 ± 4.3 mV). The maximum rise slope was 84.7 ± 11.2 mV/ms in Nav1.8 (+/+) neurons, significantly
faster than in Nav1.8 (/) neurons where it
was 47.2 ± 1.3 mV/ms. Calculations based on the action potential overshoot in Nav1.8 (+/+) and (/) neurons,
following blockade of Ca2+ currents, indicate
that Nav1.8 contributes a substantial fraction (80-90%) of the inward membrane current that flows during the rising
phase of the action potential. We found that fast TTX-sensitive Na+ channels can produce all-or-none action
potentials in some Nav1.8 (/) neurons but,
presumably as a result of steady-state inactivation of these channels,
electrogenesis in Nav1.8 (/) neurons is more sensitive to membrane depolarization than in
Nav1.8 (+/+) neurons, and, in the absence of
Nav1.8, is attenuated with even modest depolarization. These observations indicate that
Nav1.8 contributes substantially to action
potential electrogenesis in C-type DRG neurons.
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