ATP-sensitive K+ channel activation provides transient protection to the anoxic turtle brain

There is wide speculation that ATP-sensitive K+ (K-ATP) channels serve a protective function in the mammalian brain, being activated during periods of energy failure. The aim of the present study was to determine if K-ATP channels also have a protective role in the anoxia-tolerant turtle brain. After ouabain administration, rates of change in extracellular K+ were measured in the telencephalon of normoxic and anoxic turtles (Trachemys scripta). The rate of K+ efflux was reduced by 50% within 1 h of anoxia and by 70% at 2 h of anoxia, and no further decrease was seen at 4 h of anoxia. The addition of the K-ATP channel blocker glibenclamide or 2,3-butanedione monoxime prevented the anoxia-induced decrease in K+ efflux during the first hour of anoxia, but the effect of these blockers was diminished at 2 h of anoxia and was not seen after 4 h of anoxia. This pattern of change in K-ATP channel blocker sensitivity can be related to a previously established temporary fall and subsequent recovery of tissue ATP during early anoxia. We suggest that activated K-ATP channels are involved in the downregulation of membrane ion permeability (channel arrest) during the initial energy crisis period but are switched off when the full anoxic state is established and tissue ATP levels have been restored. We also found that, in contrast to those in mammals, K-ATP channels are not a major route for K+ efflux in the energy-depleted turtle brain.