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Previous Article | Next Article
Volume 17, Number 10, Issue of May 15, 1997 pp. 3503-3514
Copyright ©1997 Society for NeuroscienceDownregulation of Tetrodotoxin-Resistant Sodium Currents and Upregulation of a Rapidly Repriming Tetrodotoxin-Sensitive Sodium Current in Small Spinal Sensory Neurons after Nerve Injury
Received Dec. 11, 1996; revised March 3, 1997; accepted March 5, 1997.
Theodore R. Cummins and Stephen G. Waxman Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, and Neuroscience Research Center, Veterans Administration Medical Center, West Haven, Connecticut 06516
Clinical and experimental studies have shown that spinal sensory neurons become hyperexcitable after axonal injury, and electrophysiological changes have suggested that this may be attributable to changes in sodium current expression. We have demonstrated previously that sodium channel
-III mRNA levels are elevated and sodium channel
Key words: sodium channel; sodium current; chronic pain; axotomy; dorsal root ganglion; excitability
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