Inhibitory mechanisms control active expiration by limiting parafacial expiratory drive.

Activity of parafacial neurons that control active expiration is heavily dependent on tonic and CO2/H+-dependent excitatory and inhibitory inputs from yet poorly defined sources. Contrary to the idea that CO2/H+ disinhibits parafacial expiratory neurons, the recent work of J. D. Silva et al. (Silva JD, Oliveira LM, Souza FC, Moreira TS, Takakura AC. J Neurophysiol 123: 1933-1943, 2020) suggests that GABAergic raphe neurons preferentially limit expiratory activity during high CO2. Here, I discuss these findings and propose a model where GABAergic raphe neurons function as CO2/H+-dependent breaks on expiratory drive.