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Cited by (84)
Endodontic Pharmacology
2010, Cohen's Pathways of the Pulp, Tenth EditionThe roles of sodium channels in nociception: Implications for mechanisms of pain
2007, PainCitation Excerpt :Nav1.7 clearly plays a crucial role in pain mechanisms, but there are substantial data implicating TTX-R sodium currents and channels in pain. TTX-R sodium currents have been found primarily in the subpopulation of small diameter sensory neurons thought to be important in nociception (Caffrey et al., 1992; Roy and Narahashi, 1992; Elliott and Elliott, 1993; Arbuckle and Docherty, 1995), suggesting they too may be good targets for the development of novel analgesics. Although it is now known there are two distinct TTX-R sodium channel isoforms expressed at high levels in DRG neurons (Nav1.8 and Nav1.9), Nav1.9 currents can be difficult to record in DRG neurons under standard whole-cell recording conditions, and it is likely the TTX-R sodium currents described in the majority of studies are conducted by Nav1.8 channels.
Chapter 2 History of Ion Channels in the Pain Sensory System
2006, Current Topics in MembranesCitation Excerpt :Nav1.8 and Nav1.9 are found both in NGF‐responsive and glial cell‐derived neurotrophic factor (GDNF)‐responsive C‐fiber neurons, most of which express the capsaicin receptor TRPV1 (Amaya et al., 2000). Consistent with this, significantly higher levels of TTX‐R currents were found in capsaicin‐sensitive DRG neurons than in the capsaicin‐insensitive ones while no difference in the levels of TTX‐S current was revealed (Arbuckle and Docherty, 1995). It is worth mentioning that expression of both Nav1.8 and Nav1.9 increases with embryonic age (Benn et al., 2001) indicating that the developmental regulation of Na+ channel expression is a complex process affecting several Na+ channel subtypes (see also Nav1.3 given earlier and Nav1.5 in the following paragraph).