The pontine respiratory group, particularly the Kolliker-Fuse nucleus, mediates phases of the hypoxic ventilatory response in unanesthetized goats

Bonis JM, Neumueller SE, Krause KL, Kiner T, Smith A, Marshall BD, Qian B, Pan LG, Forster HV. The pontine respiratory group, particularly the Kolliker-Fuse nucleus, mediates phases of the hypoxic ventilatory response in unanesthetized goats. J Appl Physiol 108: 1321-1335, 2010. First published February 18, 2010; doi: 10.1152/japplphysiol.00935.2009.-The objective of the present study was to test the hypothesis that, in the in vivo awake goat model, perturbation/lesion in the pontine respiratory group (PRG) would decrease the sensitivity to hypercapnia and hypoxia. The study reported herein was part of two larger studies in which cholinergic modulation in the PRG was attenuated by microdialysis of atropine and subsequently ibotenic acid injections neurotoxically lesioned the PRG. In 14 goats, cannula were bilaterally implanted into either the lateral (n = 4) or medial (n = 4) parabrachial nuclei or the Kolliker-Fuse nucleus (KFN, n = 6). Before and after cannula implantation, microdialysis of atropine, and injection of ibotenic acid, hypercapnic and hypoxic ventilatory sensitivities were assessed. Hypercapnic sensitivity was assessed by three 5-min periods at 3, 5, and 7% inspired CO2. In all groups of goats, CO2 sensitivity was unaffected (P > 0.05) by any PRG perturbations/lesions. Hypoxic sensitivity was assessed with a 30-min period at 10.8% inspired O-2. The response to hypoxia was typically triphasic, with a phase 1 increase in pulmonary ventilation, a phase 2 roll-off, and a phase 3 prolonged increase associated with shivering and increased metabolic rate and body temperature. In all groups of goats, the phase 1 of the hypoxic ventilatory responses was unaffected by any PRG perturbations/lesions, and there were no consistent effects on the phase 2 responses. However, in the KFN group of goats, the phase 3 ventilatory, shivering, metabolic rate, and temperature responses were markedly attenuated after the atropine dialysis studies, and the attenuation persisted after the ibotenic acid studies. These findings support an integrative or modulatory role for the KFN in the phase 3 responses to hypoxia.