Electrophysiological recordings were obtained from rat dorsal roots in a sucrose gap chamber to study changes in Na(+) currents following nerve injury. Application of 4-aminopyridine unmasks a prominent and well-characterized depolarization (delayed depolarization) following the action potential. In our previous studies, this potential, which is only present in cutaneous afferent axons, has been shown to correlate with activation of a slow Na(+) current. The delayed depolarization in the dorsal root was reduced 1 week after sciatic nerve ligation, suggesting a reduction in the kinetically slow Na(+) currents on dorsal root axons [control: 44. 2+/-7.3% (n=5); injury: 7.3+/-4.7% (n=5), P<0.001]. The refractory period of the action potential was reduced following nerve injury, in agreement with biophysical studies indicating faster "repriming" of fast Na(+) currents on cutaneous afferent cell bodies. Dorsal root ligation near the spinal cord also results in a reduction in the delayed depolarization. These results indicate that changes in Na(+) channel organization occur on dorsal root axons following either central or peripheral target disconnection, suggesting trophic support can be derived from either the CNS or the PNS.