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Vol. 84, Issue 1, 129-140, January 1998
Departments of Physiology and Pediatrics, Medical College of Wisconsin; Program in Physical Therapy, Marquette University; and Zablocki Veterans Medical Center, Milwaukee, Wisconsin 53226
Forster, H. V., L. G. Pan, T. F. Lowry, T. Feroah, W. M. Gershan, A. A. Whaley, M. M. Forster, and B. Sprtel. Breathing of
awake goats during prolonged dysfunction of caudal M ventrolateral medullary neurons. J. Appl. Physiol.
84(1): 129-140, 1998.
Cooling the caudal M ventrolateral
medullary (VLM) surface for 30 s results in a sustained apnea in
anesthetized goats but only a 30% decrease in breathing in awake
goats. The purpose of the present study was to determine, in the awake
state, the effect of prolonged (minutes, hours) caudal M neuronal
dysfunction on eupneic breathing and
CO2 sensitivity. Dysfunction was
created by ejecting excitatory amino acid receptor antagonists or a
neurotoxin on the VLM surface through guide tubes chronically implanted
bilaterally on a 10- to 12-mm2
portion of the caudal M VLM surface of 12 goats. Unilateral and bilateral ejections (1 µl) of selective antagonists for
N-methyl-D-aspartic acid or
non-N-methyl-D-aspartic
acid receptors had no significant effect on eupneic breathing or
CO2 sensitivity. Unilateral
ejection of a nonselective excitatory amino acid receptor antagonist
generally had no effect on eupneic breathing or
CO2 sensitivity. However, bilateral ejection of this antagonist resulted in a significant 2-Torr
hypoventilation during eupnea and a significant reduction in
CO2 sensitivity to 60 ± 9% of
control. Unilateral ejection of the neurotoxin kainic acid initially
stimulated breathing; however, breathing then returned to near control
with no incidence of apnea. After the kainic acid ejection,
CO2 sensitivity was reduced
significantly to 60 ± 7% of control. We conclude that in the awake
state a prolonged dysfunction of caudal M VLM neurons results in
compensation by other mechanisms (e.g., carotid chemoreceptors, wakefulness) to maintain near-normal eupneic breathing, but
compensation is more limited for maintaining
CO2 sensitivity.
regulation of breathing; excitatory amino acid receptors; ventrolateral medulla
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