We hypothesize that breathing in mammals results from interactions between two oscillators: the preBötzinger Complex (preBötC) is the kernel for inspiration, while the retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) is vital for active expiration and CO2 chemoreception. We functionally dissected the RTN/pFRG by transfecting different populations of neighboring neurons with allatostatin or HM4D (DREADD) Gi/o-coupled receptors, and then analyzed the effect of their hyperpolarization on breathing in adult rats [1]. We identified two functionally separate parafacial nuclei: ventral (pFV) and lateral (pFL). We conclude that the pFV provides a generic excitatory drive to breathe, even at rest, whereas the pFL is a conditional oscillator quiet at rest that, when activated, e.g., during exercise, drives active expiration. We then looked at the interactions between the preBötC and pFL, by independently altering their excitability in adult rats [2]. Hyperpolarizing preBötC neurons decreased inspiratory activity and initiated active expiration, before ultimately progressing to apnea, i.e., cessation of both inspiration and active expiration. Depolarizing pFL neurons produced active expiration at rest, but not when inspiratory activity was suppressed by hyperpolarizing preBötC neurons. We conclude that in adult rats active expiration is driven by the pFL but requires an additional form of network excitation, i.e., ongoing rhythmic preBötC activity sufficient to drive inspiratory motor output or increased chemosensory drive. The organization of this coupled oscillator system, which is essential for life, may have implications for other neural networks that contain multiple rhythm/pattern generators.