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Departments of Physiology and Pediatrics, Medical College of Wisconsin, Milwaukee 53226; Program in Physical Therapy, Marquette University, Milwaukee 53295; and Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53226
The purpose of this study was to determine the effect on
breathing of neuronal dysfunction in the retrotrapezoid (RTN), facial (FN), gigantocellularis reticularis (RGN), or vestibular (VN) nuclei of
adult awake goats. Microtubules were chronically implanted to induce
neuronal dysfunction by microinjection of an excitatory amino acid
(EAA) receptor antagonist or a neurotoxin. 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 significant (P > 0.10) effects of the
EAA receptor antagonist on CO2 sensitivity. However, for
all nuclei,
66% of the antagonist injections altered CO2
sensitivity by more than the normal 12.7 ± 1.6% day-to-day
variation. These changes were not uniform, inasmuch as the antagonist
increased (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 the neurotoxin into the FN (n = 3) or RGN
(n = 5), CO2 sensitivity was also reduced.
Neuronal dysfunction also did not have a uniform effect on the exercise arterial PCO2 response, and there was no
correlation between effects on CO2 sensitivity and the
exercise hyperpnea. We conclude that there is a heterogeneous
population of neurons in these rostral medullary nuclei (or adjacent
tissue) that can affect breathing in the awake state, possibly through
chemoreception or chemoreceptor-related mechanisms.
rostral medulla; excitatory amino acid receptors; carbon dioxide sensitivity; exercise
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