Introduction: In retrotrapezoid nucleus neurons, inhibition of TASK2 by extracellular and/or intracellular protons (as a proxy for blood [CO2]) depolarizes the cell, increases spike frequency and leads to increased respiration. To determine how TASK2 replys to the change of CO2 concentration and regulate respiration, we reconstituted TASK2 into nanodiscs under different pH and captured the open and closed TASK2 structures respectively by cyro-electron microscopy. With the use of electrophysiology methods and biochemical experiments, we systematically clarified the mechanism of TASK2 as a pH receptor of chemorecepting in central neural system, which well promoted the understanding of how central chemoreceptors regulate respiration and the gating mechanism of ion channels.
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