Ventrolateral pons mediates short-term depression of respiratory frequency after brief hypoxia.

The respiratory response to hypoxia is dynamic in the adult anesthetized Sprague-Dawley rat. Hypoxia elicits acute increases in both tidal volume (VT) and respiratory frequency (fR) followed by short-term increases in VT and short-term decreases in fR. After brief hypoxia (<1 min), recovery of the breathing pattern is again dynamic, where both VT and fR decrease immediately, but where VT remains above, and fR drops below, baseline. These acute changes are followed by a short-term progressive decrease in VT and increase in fR to baseline. We have identified a potential neural mechanism that depends on the integrity of the ventrolateral (vl) pons. Our studies show that: (a) blockade of activity in the vl pons prevents the short-term decrease in fR after hypoxia (b) stimulation of the vl pons decreases fR, and (c) vl pontine expiratory neurons are activated after hypoxia. These neurons may not be acting through alpha(2) -adrenergic receptors, but their effect does depend on NMDA-type receptor function. We conclude that the vl pons is a critical element in the pontomedullary network that generates and modulates the fR response to acute hypoxia.