Changes in nerve membrane polarization following repeated exposure to soman

Abstract

The purpose of this study was to determine whether the slowly developing changes in potassium‐induced depolarization in nerve membrane produced by soman are due to blockade of potassium conductance or to inhibition of Na,K‐ATPase. Rats were dosed daily for 20 d with soman (0.075 mg/kg, ip). In isolated sucrose gap chambers, the nerves were challenged with extracellular potassium in the presence and absence of ouabain, 4‐aminopyridine, and ouabain plus 4‐aminopyridine. The enhancement of potassium‐induced depolarization produced individually by ouabain and 4‐aminopyridine was unaffected by soman pretreatment of the nerves. However, in the presence of both ouabain and 4‐aminopyridine the soman‐treated nerves showed a marked enhancement of potassium‐induced depolarization. This effect was not seen in nerves exposed to soman for only 1 d. These results show that soman affects a nerve‐membrane process other than potassium channels or Na,K‐ATPase. The role of this unidentified process apparently is important in maintaining nerve function only when potassium conductance is blocked and Na,K‐ATPase is inhibited. Furthermore, the effect of soman on this process is the result of an adaptive change rather than a direct effect, since single‐dose exposure produced no shift in potassium‐induced depolarization.