Fig. 13.

Proposed interactions between BötC/pre-BötC and RTN/pFRG oscillators in adult mammals in vivo. Red arrows represent excitatory influence; blue lines terminated with circles indicate inhibitory influence; violet arrows indicate metabolic dependence. Under normal metabolic conditions, the RTN/pFRG oscillator is inhibited by the BötC/pre-BötC oscillator (the core of the respiratory CPG) during both inspiration (by the inhibitory early-I neurons of pre-BötC) and expiration (by the post-I neurons of BötC) and remains silent. The normal expression of post-I inhibition requires excitatory drive from the pons (not shown). The RTN/pFRG oscillator can be activated either by hypercapnia, which directly excites RTN/pFRG neurons, or by hypoxia/anoxia (or pontine suppression), which reduces RTN/pFRG inhibition by the BötC/pre-BötC oscillator, or by both. When activated, the RTN/pFRG oscillator provides both excitation of the BötC/pre-BötC oscillator and inhibition of rVRG premotor neurons, hence increasing the delay between hypoglossal and phrenic discharges.