Differential effects of an NMDA and a non-NMDA receptor antagonist on medullary lateral tegmental field neurons

The view that non-NMDA and NMDA receptors are involved in setting the basal level of activity of LTF sympathoexcitatory neurons and in synchronizing their discharges to the AP, respectively is supported.

Abstract

We microiontophoresed an N-methyl-D-aspartate (NMDA) and a non-NMDA receptor antagonist onto medullary lateral tegmental field (LTF) neurons, the naturally occurring discharges of which were correlated to the cardiac-related rhythm in sympathetic nerve discharge (SND) of dialurethane-anesthetized cats. Some of these neurons were classified as sympathoexcitatory, because their firing rate decreased during baroreceptor reflex activation. Microiontophoresis of 1,2,3,4-tetrahydro-6-nitro-2,3-dioxobenzo-[f]quinoxaline-7-sulfonamide (NBQX), a non-NMDA receptor antagonist, reduced the mean firing rates of these neurons (51 +/- 8% of control, P < 0.001, n = 20) without affecting their relationship to cardiac-related SND, as indicated by the lack of significant changes in the ratio of peak to background counts in arterial pulse (AP)-triggered histograms of LTF neuronal activity and the AP-LTF coherence value at the frequency of the heartbeat. In contrast, microiontophoresis of D(-)-2-amino-5-phosphonopentanoic acid, an NMDA receptor antagonist, onto LTF neurons reduced the ratio of peak to background counts in AP-triggered histograms to 57 +/- 9% of control (P = 0.002, n = 16) and the AP-LTF coherence value to 25 +/- 10% of control (P = 0.001, n = 10). These data support the view that non-NMDA and NMDA receptors are involved in setting the basal level of activity of LTF sympathoexcitatory neurons and in synchronizing their discharges to the AP, respectively.