Excitability changes of dorsal root axons following nerve injury: implications for injury-induced changes in axonal Na + channels

Abstract

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.