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Cholinergic control of ventral surface chemoreceptors involves Gq/inositol 1,4,5‐trisphosphate‐mediated inhibition of KCNQ channels

ACh is an important modulator of breathing, including at the level of the retrotrapezoid nucleus (RTN), where evidence suggests that ACh is essential for the maintenance of breathing. Despite this potentially important physiological role, little is known about the mechanisms responsible for the cholinergic control of RTN function. In the present study, we show at the cellular level that ACh increases RTN chemoreceptor activity by a CO2/H+ independent mechanism involving M1/M3 receptor‐mediated inositol 1,4,5‐trisphosphate/Ca+2 signalling and downstream inhibition of KCNQ channels. These results dispel the theory that ACh is required for RTN chemoreception by showing that ACh, similar to serotonin and other modulators, controls the activity of RTN chemoreceptors without interfering with the mechanisms by which these cells sense H+. By identifying the mechanisms by which wake‐on neurotransmitters such as ACh modulate RTN chemoreception, the results of the present study provide a framework for understanding the molecular basis of the sleep–wake state‐dependent control of breathing.