Differential Changes of ATP-sensitive Potassium Channel Current after Hypoxia-reperfusion Treatment in Mouse Neuroblastoma 2a (N2a) Cell

Differential Changes of ATP-sensitive Potassium Channel Current after Hypoxia-reperfusion Treatment in Mouse Neuroblastoma 2a (N2a) Cell

<P> Ischemic damage is one of the most serious problems. The openers of K<SUB>ATP</SUB> channel have been suggested to have an effect to limit the ischemic damage. However, it is not yet clear how K<SUB>ATP</SUB> channels of a cell correspond to hypoxic damage. To address the question, N2a cells were exposed to two different hypoxic conditions as follows: 6 hours hypoxia followed by 3 hours reperfusion and 12 hours hypoxia followed by 3 hours reperfusion. As the results, 6 hours hypoxic treatment increased glibenclamide- sensitive basal K<SUB>ATP</SUB> current activity (approximately 6.5-fold at 0 mV test potential) when compared with nomoxic condition. In contrast, 12 hours hypoxic treatment induced a relatively smaller change in the K<SUB>ATP</SUB> current density (2.5-fold at 0 mV test potential). Additionally, in experiments where K<SUB>ATP</SUB> channels were opened using diazoxide, the hypoxia for 6 hours significantly increased the current density in comparison to control condition (p＜0.001). Interestingly, the augmentation in the K<SUB>ATP</SUB> current density reduced after exposure to the 12 hours hypoxic condition (p＜0.001). Taken together, these results suggest that K<SUB>ATP</SUB> channels appear to be recruited more in cells exposed to the 6 hours hypoxic condition and they may play a protective role against hypoxia-reperfusion damage within the time range.