Under extreme environmental conditions, many insects enter a protective coma associated with a spreading depolarization (SD) of neurons and glia in the central nervous system (CNS). Recovery depends on the restoration of ion gradients by mechanisms that are not well understood. We investigated the effects of glybenclamide, an ATP-sensitive K (K) channel inhibitor, and pinacidil, a K activator, on the mechanisms involved in anoxic coma induction and recovery in . K channels allow for the efflux of K when activated, thereby linking cellular metabolic state to membrane potential. In intact locusts, we measured the time to enter a coma after water immersion and the time to recover the righting reflex after returning to normoxia. In semi-intact preparations, we measured the time to SD in the metathoracic ganglion after flooding the preparation with saline or exposing it to 100% N gas, and the time for the transperineurial potential to recover after removal of the saline or return to air. Glybenclamide decreased the time to coma induction, whereas pinacidil increased induction times. Glybenclamide also lengthened the time to recovery and decreased the rate of recovery of transperineurial potential after SD. These results were not the same as the effects of 10 M ouabain on N-induced SD. We conclude that glybenclamide affects the CNS response to anoxia via inhibition of K channels and not an effect on the Na/K-ATPase. We demonstrate the involvement of ATP-sensitive K (K) channels during recovery from spreading depolarization (SD) induced via anoxic coma in locusts. K inhibition using glybenclamide impaired ion homeostasis across the blood-brain barrier resulting in a longer time to recovery of transperineurial potential following SD. Comparison with ouabain indicates that the effects of glybenclamide are not mediated by the Na/K-ATPase but are a result of K channel inhibition.
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