Key result
Microinjection of a neurotoxin into rostral medullary nuclei caused hypoventilation in 7 of 10 awake goats (arterial PCO2 increased 3.2 +/- 0.7 Torr) and altered CO2 sensitivity.
p-value: p=> 0.10
Neuronal dysfunction in rostral medullary nuclei alters breathing and CO2 sensitivity in awake goats, indicating a heterogeneous population of neurons affecting respiration.
Hypothesis-generating for rostral medullary contributions to awake ventilatory control; human studies required before clinical translation.
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 PCO(2) increased 3.2 +/- 0.7 Torr). Overall there were no significant (P > 0.10) effects of the EAA receptor antagonist on CO(2) sensitivity. However, for all nuclei, > or =66% of the antagonist injections altered CO(2) 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) CO(2) sensitivity. Ten days after injection of the neurotoxin into the FN (n = 3) or RGN (n = 5), CO(2) sensitivity was also reduced. Neuronal dysfunction also did not have a uniform effect on the exercise arterial PCO(2) response, and there was no correlation between effects on CO(2) 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.
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Wenninger et al. (2001) studied Breathing regulation in awake goats (n=10). Microinjection of an excitatory amino acid (EAA) receptor antagonist or a neurotoxin was evaluated on CO2 sensitivity and eupneic breathing (p=> 0.10). Microinjection of a neurotoxin into rostral medullary nuclei caused hypoventilation in 7 of 10 awake goats (arterial PCO2 increased 3.2 +/- 0.7 Torr) and altered CO2 sensitivity.
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