Voltage-dependent Na+ channels in sensory nerves contribute to the control
of membrane excitability and underlie action potential generation. Na+ chan
nel subtypes exhibit a neurone-specific and developmentally regulated patte
rn of expression, and changes in both channel expression and function are c
aused by disease. Recent evidence implicates specific roles for Na+ channel
subtypes Na(v)1.3 and Na(v)1.8 in pain states that are associated with ner
ve injury and inflammation, respectively. Insight into the role of Na(v)1.8
in pain pathways has been gained by the generation of a null mutant. Altho
ugh drugs discriminate poorly between subtypes, the molecular diversity of
channels and subtype-specific modulation might provide opportunities to tar
get pain pathways selectively.