title: 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.
authors.affiliation: Ottawa Civic Hospital Loeb Medical Research Institute, Division of Neuroscience, University of Ottawa, Ont, Canada.
authors.forename: P K
authors.initials: PK
authors.lastname: Stys
authors.forename: D A
authors.initials: DA
authors.lastname: Hubatsch
authors.forename: L L
authors.initials: LL
authors.lastname: Leppanen
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000704:Analysis of Variance; D000818:Animals; D001369:Axons / Q000187:drug effects*; D002534:Hypoxia, Brain / Q000188:drug therapy*; D008564:Membrane Potentials / Q000187:drug effects; D009186:Myelin Sheath / Q000187:drug effects*; D009900:Optic Nerve / Q000187:drug effects*; D026902:Potassium Channel Blockers; D051381:Rats
chemical_list: D026902:Potassium Channel Blockers