Effects of K+ channel blockers on the anoxic response of CNS myelinated axons.

Abstract

Compound action potentials (CAPs) from adult rat optic nerves were recorded in vitro. The area under the CAP was compared before and after 1 h anoxia/reoxygenation. Resting compound membrane potential was measured using the cold grease-gap technique. The acute reduction of CAP magnitude by anoxia was unaffected by TEA (20 mM), 4-AP (300 microM), or the KATP blockers glibenclamide (300 microM) and tolbutamide (2 mM). Neither these K+ channel blockers, nor glipizide (100 microM) or the KATP activator diazoxide (500 microM) altered post-anoxic CAP area recovery. In contrast, although Cs+ (5 mM) accelerated anoxic CAP failure and membrane depolarization, this cation significantly increased CAP area recovery post-anoxia from 22+/-10% (s.d.) to 60+/-22% (p < 0.0001). The unique effects of Cs+ suggest that inward rectifier channels may play an important role in the induction of anoxic injury in optic nerve axons.