Differential expression of ion channels contributes functional diversity to
sensory neuron signaling. We find nerve injury induced by the Chung model
of neuropathic pain leads to striking reductions in voltage-gated K+ (Kv) c
hannel subunit expression in dorsal root ganglia (DRG) neurons, suggesting
a potential molecular mechanism for hyperexcitability of injured nerves. Mo
reover, specific classes of DRG neurons express distinct Kv channel subunit
combinations. Importantly, Kv1.4 is the sole Kv1 alpha subunit expressed i
n smaller diameter neurons, suggesting that homomeric Kv1.4 channels predom
inate in A delta and C fibers arising from these cells. These neurons are p
resumably nociceptors, because they also express the VR-1 capsaicin recepto
r, calcitonin gene-related peptide, and/or Na+ channel SNS/PN3/Nav1.8. In c
ontrast, larger diameter neurons associated with mechanoreception and propr
ioception express high levels of Kv1.1 and Kv1.2 without Kv1.4 or other Kv1
alpha subunits, suggesting that heteromers of these subunits predominate o
n large, myelinated afferent axons that extend from these cells.