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1 Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48824; and 2 Department of Pharmacology, Faculty of Medicine, Hacettepe University, 06100 Ankara, Turkey
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.
cardiac-related activity; excitatory amino acid neurotransmission; sympathetic nerve discharge; sympathoexcitatory neurons
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