Moreover, in a working heart-brainstem preparation, TASK-2 KO blunted inhibition of phrenic nerve burst amplitude during respiratory alkalosis and increased the pH threshold for apnea.47 In their TASK-2 KO mouse model, Gestreau et al reported that TASK-2 stabilizes the membrane potential of central chemoreceptive cells.46 They found that hypoxia-induced respiratory depression was abolished in TASK-2 KO mice, and hypothesized that TASK-2 activation by reactive oxygen species which are generated in hypoxia could silence the RTN neurons, as a basis for this respiratory depression. Here, KCNK5 is linked to respiratory depression.