Abstract
The brain regulates breathing in response to changes in CO(2)/H(+) by a process referred to as respiratory chemoreception. The retrotrapezoid nucleus (RTN) is essential for this function. RTN neurons are intrinsically activated by CO(2)/H(+). Astrocytes contribute as well, by providing a CO(2)/H(+)-dependent purinergic drive to augment neural activity directly and indirectly by causing vasoconstriction. Here, we summarize preclinical studies in rodents that identify: (i) mechanisms of CO(2)/H(+) detection by RTN neurons; (ii) how this information is integrated at the neural network level; and (iii) how RTN neural activity is shaped by CO(2)/H(+) sensitive astrocytes. We also discuss how disruption of RTN chemoreception might contribute to breathing problems in disease, and highlight the therapeutic potential of targeting CO(2)/H(+)-dependent and -independent regulatory elements of RTN neurons.