Blockade of N-methyl-D-aspartate receptors has no effect on certain inspiratory reflexes.

Previous studies have indicated that excitatory amino acids are involved in many afferent pathways. This study investigated the effects of intravenous MK-801 [an N-methyl-D-aspartate (NMDA) receptor-associated channel blocker] on several well-known respiratory reflexes elicited by afferent stimulation of the superior laryngeal (SLN), the intercostal (ICN), and the phrenic (PN) nerves. Control responses to stimulation were obtained from recordings of phrenic nerve activity in decerebrate, paralyzed cats. Inspiratory termination elicited by the delivery of stimulus trains to either the SLN or the ICN persisted after MK-801. The onset latency or duration of the short-latency excitations produced by SLN or ICN stimulation were unchanged. The transient inhibitions produced by SLN, ICN, PN, or medullary stimulation showed no significant changes in threshold, onset latency, or duration. Withholding lung inflation produced apneusis after administration of MK-801, indicating a central effect of the drug. Higher doses of MK-801 did not alter the parameters of these reflexes. These data indicate that NMDA-dependent neurotransmission is not required for the production of these reflexes.