Electrophysiologic deficits in peripheral nerve as a discriminator of early hexacarbon neurotoxicity

Abstract

To determine the extent of neurotoxicity of parenterally administered hexacarbons, male Sprague‐Dawley rats were given either n‐hexane or 2,5‐hexanedione for 35 consecutive days. Electrophysiologic measurements showed a lengthening of the sciatic and sural nerve action potentials (slower conduction velocities) and increased refractory periods. These effects correlated with a shift in the nerve membrane sensitivity to potassium‐induced depolarization. A similar effect can be induced by ouabain, an Na⁺, K⁺ A TPase inhibitor. These effects were seen with both n‐hexane and 2,5‐hexanedione. Although the treated animals gained wieght more slowly than controls, they showed no loss of motor function when tested behaviorally, and there were no signs of histopathology in the peripheral nerves. These results show that hexacarbons produce a neurotoxocity that can be demonstrated by changes in nerve excitability, prior to overt behavioral neurotoxocity. Furthermore, these electrophysiologic changes may be related to a hexacarbon‐induced disruption of nerve‐membrane A TPase activity.