BREATHING OF AWAKE GOATS DURING PROLONGED DYSFUNCTION OF CAUDAL M-VENTROLATERAL MEDULLARY NEURONS

Cooling the caudal M ventrolateral medullary (VLM) surface for 30 s re sults in a sustained apnea in anesthetized goats but only a 30% decrea se in breathing in awake goats. The purpose of the present study was t o determine, in the awake state, the effect of prolonged (minutes, hou rs) caudal M neuronal dysfunction on eupneic breathing and CO2 sensiti vity. Dysfunction was created by electing excitatory amino acid recept or antagonists or a neurotoxin on the VLM surface through guide tubes chronically implanted bilaterally on a 10- to 12-mm(2) portion of the caudal M VLM surface of 12 goats. Unilateral and bilateral ejections ( 1 mu l) 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 e xcitatory amino acid receptor antagonist generally had no effect on eu pneic breathing or CO2 sensitivity. However, bilateral ejection of thi s antagonist resulted in a significant 2-Torr hypoventilation during e upnea and a significant reduction in CO2 sensitivity to 60 +/- 9% of c ontrol. Unilateral ejection of the neurotoxin kainic acid initially st imulated breathing; however, breathing then returned to near control w ith no incidence of apnea. After the kainic acid ejection, CO2 sensiti vity was reduced significantly to 60 +/- 7% of control. We conclude th at in the awake state a prolonged dysfunction of caudal M VLM neurons results in compensation by other mechanisms (e.g., carotid chemorecept ors, wakefulness) to maintain near-normal eupneic breathing, but compe nsation is more limited for maintaining CO2 sensitivity.