The purpose of this study was to determine the effect on breathing of neuro
nal dysfunction in the retrotrapezoid (RTN), facial (FN), gigantocellularis
reticularis (RGN), or vestibular (VN) nuclei of adult awake goats. Microtu
bules were chronically implanted to induce neuronal dysfunction by microinj
ection of an excitatory amino acid (EAA) receptor antagonist or a neurotoxi
n. The EAA receptor antagonist had minimal effect on eupneic breathing, but
8-10 days after injection of the neurotoxin, 7 of 10 goats hypoventilated
(arterial PCO2 increased 3.2 +/-0.7 Torr). Overall there were no significan
t (P > 0.10) effects of the EAA receptor antagonist on CO2 sensitivity. How
ever, for all nuclei, greater than or equal to 66% of the antagonist inject
ions altered CO2 sensitivity by more than the normal 12.7 +/-1.6% day-to-da
y variation. These changes were not uniform, inasmuch as the antagonist inc
reased (RTN, n = 2; FN, n = 7; RGN, n = 6; VN, n = 1) or decreased (RTN, n
= 2; RGN, n = 3; VN, n = 2) CO2 sensitivity. Ten days after injection of th
e neurotoxin into the FN (n = 3) or RGN (n = 5), CO2 sensitivity was also r
educed. Neuronal dysfunction also did not have a uniform effect on the exer
cise arterial PCO2 response, and there was no correlation between effects o
n CO2 sensitivity and the exercise hyperpnea. We conclude that there is a h
eterogeneous population of neurons in these rostral medullary nuclei (or ad
jacent tissue) that can affect breathing in the awake state, possibly throu
gh chemoreception or chemoreceptor-related mechanisms.