Under extreme environmental conditions, many insects enter a protective coma associated with a spreading depolarization (SD) of neurons and glia in the 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_ATP) channel inhibitor, and pinacidil, a K_ATP activator, on the mechanisms involved in anoxic coma induction and recovery in Locusta migratoria. K_ATP 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 % N₂ 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^-2 M ouabain on N₂-induced SD. We conclude that glybenclamide affects the CNS response to anoxia via inhibition of K_ATP channels and not an effect on the Na⁺/K⁺-ATPase.

中文翻译：

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ATP 敏感钾通道的抑制加剧了蝗虫的缺氧昏迷

在极端环境条件下，许多昆虫进入保护性昏迷，与中枢神经系统中神经元和神经胶质的扩散去极化 (SD) 相关。恢复取决于通过尚未完全了解的机制恢复离子梯度。我们研究了甘苯脲（一种 ATP 敏感的 K ⁺ (K _ATP ) 通道抑制剂）和吡那地尔（一种 K _ATP激活剂）对蝗虫缺氧昏迷诱导和恢复机制的影响。K _ATP通道允许 K ⁺外流当被激活从而将细胞代谢状态与膜电位联系起来时。在完整的蝗虫中，我们测量了浸水后进入昏迷的时间和恢复常氧后恢复翻正反射的时间。在半完整制剂中，我们测量了用盐水淹没制剂或将其暴露于 100% N ₂气体后后胸神经节到 SD 的时间，以及去除盐水或返回空气后经神经膜电位恢复的时间. 格列本脲减少昏迷诱导时间，而吡那地尔增加诱导时间。格列本脲还延长了恢复时间并降低了 SD 后经神经膜电位的恢复率。这些结果与 10 ^-2 Mouabain 对 N 的影响不同_2-诱导的SD。我们得出结论，格列本脲通过抑制 K _ATP通道而不影响 Na ⁺ /K ⁺ -ATPase来影响 CNS 对缺氧的反应。