Adrenergic C1 neurons are part of the circuitry that recruits active expiration in response to hypoxia

Abstract

AbstractBreathing results from the interaction of two distinct oscillators: the preBötzinger Complex (preBötC) driving inspiration and the lateral parafacial region (pFRG) driving active expiration. The pFRG is silent during resting and become rhythmically active during high metabolic demand such as hypoxia. Catecholaminergic C1 cells are activated by hypoxia, which is a strong stimulus for active expiration. We hypothesized that the C1 cells and pFRG may constitute functionally distinct but interacting populations in order to contributes to control expiratory activity during hypoxia. We found that: a) C1 neurons are activated by hypoxia and project to pFRG region; b) active expiration elicited by hypoxia was blunted after blockade of ionotropic glutamatergic antagonist at the level of pFRG and c) selective depletion of C1 neurons eliminated the active expiration elicited by hypoxia. The results suggest that C1 cells may regulate the respiratory cycle including the active expiration under hypoxic condition.