Accumulating myelin abnormalities and conduction slowing occur in peripheral nerves during aging. In mice deficient of myelin protein P₀, severe peripheral nervous system myelin damage is associated with ectopic expression of Na_v1.8 voltage-gated Na⁺ channels on motor axons aggravating the functional impairment. The aim of the present study was to investigate the effect of regular aging on motor axon function with particular emphasis on Na_v1.8. We compared tibial nerve conduction and excitability measures by threshold tracking in 12 months (mature) and 20 months (aged) wild-type (WT) mice. With aging, deviations during threshold electrotonus were attenuated and the resting current-threshold slope and early refractoriness were increased. Modeling indicated that, in addition to changes in passive membrane properties, motor fibers in aged WT mice were depolarized. An increased Na_v1.8 isoform expression was found by immunohistochemistry. The depolarizing excitability features were absent in Na_v1.8 null mice, and they were counteracted in WT mice by a Na_v1.8 blocker. Our data suggest that alteration in voltage-gated Na⁺ channel isoform expression contributes to changes in motor axon function during aging.