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

• Published in: Neuroreport Vol. 9; no. 3; p. 447
• Main Authors: Stys, P K, Hubatsch, D A, Leppanen, L L
• Format: Journal Article
• Language: English
• Published: England 16.02.1998
• Subjects: Action Potentials - drug effects; Analysis of Variance; Animals; Axons - drug effects; Hypoxia, Brain - drug therapy; Membrane Potentials - drug effects; Myelin Sheath - drug effects; Optic Nerve - drug effects; Potassium Channel Blockers; Rats
• ISSN: 0959-4965
• DOI: 10.1097/00001756-199802160-00017

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.