Background and Purpose - In light of recent evidence suggesting that an upregulation of K+ efflux mediated by outward delayed rectifier (IK) channels promotes central neuronal apoptosis, we sought to test the possibility that blockers of IK channels might be neuroprotective against hypoxia/ischemia-induced neuronal death. Methods - Membrane currents were recorded with the use of patch clamp recordings in cultured murine cortical neurons. Protective effects of K+ channel blockers were examined in rats subjected to transient middle cerebral artery occlusion followed by 14-day reperfusion. Results - The K+ channel blocker tetraethylammonium (TEA) (5 mmol/L) selectively blocked IK without affecting N-methyl-D-aspartate receptor - mediated current or voltage-gated Ca2+ currents. Both TEA and a lipophilic K+ channel blocker, clofilium, attenuated neuronal apoptosis induced by hypoxia in vitro and infarct volume induced by ischemia in vivo. Conclusions - These data are consistent with the idea that K+ channel-mediated K+ efflux may contribute to ischemia-triggered apoptosis and suggest that preventing excessive K+ efflux through K+ channels may constitute a therapeutic approach for the treatment of stroke.

Original languageEnglish
Pages (from-to)1281-1286
Number of pages6
Issue number5
StatePublished - May 1 2003


  • Hypoxia
  • Ischemia
  • Middle cerebral artery occlusion
  • Tetraethylammonium


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