THE DELAYED DEPOLARIZATION IN RAT CUTANEOUS AFFERENT AXONS IS REDUCEDFOLLOWING NERVE TRANSECTION AND LIGATION, BUT NOT CRUSH - IMPLICATIONS FOR INJURY-INDUCED AXONAL NA+ CHANNEL REORGANIZATION

Two distinct populations of Na+ channels (kinetically fast and slow) a re present on the cell bodies and axons of cutaneous efferent neurons; the fast current is increased and the slow current reduced in amplitu de following nerve injury. The present study was undertaken to determi ne if similar changes occur on the axons of these neurons following pe ripheral nerve injury. The compound action potentials from rat sural n erves were recorded in a sucrose gap chamber. Following application of 4-aminopyridine, a prominent and well-characterized depolarization (t he delayed depolarization) followed the action potential. This potenti al, only present on cutaneous afferent axons, has been correlated with activation of a slow Na(+ )current. The delayed depolarization was re duced after nerve transection. The refractory period of transmission o f the action potential was shortened in the transected nerves, but tha t of the delayed depolarization was prolonged. The changes were larges t when the sural nerve was cut and ligated [control: 38.1 +/- 1.7% (n = 5); injury: 24.5 +/- 2.8% (n = 5), P < 0.05], which prevented reconn ection to its peripheral target. When the nerve was crushed and allowe d to reestablish peripheral target connections, the delayed depolariza tion was minimally effected. These results indicate that the changes i n Na+ channel organization following peripheral target disconnection o bserved on cutaneous afferent cell bodies also occur on their axons. ( C) 1998 John Wiley & Sons, Inc.