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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
This study was designed to test the
hypothesis that the medullary lateral tegmental field (LTF) is an
important synaptic relay in the baroreceptor reflex pathway controlling
sympathetic nerve discharge (SND) of urethan-anesthetized cats. We
determined the effects of blockade of excitatory amino acid-mediated
neurotransmission in the LTF on three indexes of baroreceptor reflex
function: cardiac-related power in SND, strength of linear correlation
(coherence value) of SND to the arterial pulse (AP), and inhibition of
SND during increased arterial pressure produced by abrupt obstruction
of the abdominal aorta. Bilateral microinjection of
D-(
)-2-amino-5-phosphonopentanoic acid, an
N-methyl-D-aspartate
(NMDA) receptor antagonist, abolished cardiac-related power and
coherence of SND to the AP, and it prevented inhibition of SND during
aortic obstruction. These data support the view that NMDA
receptor-mediated neurotransmission in the LTF is critical for
baroreceptor reflex control of SND. Bilateral microinjection of
1,2,3,4-tetrahydro-6-nitro-2,3-dioxobenzo-[f]-quinoxaline-7-sulfonamide, a non-NMDA receptor antagonist, decreased cardiac-related power and
total power in the 0- to 6-Hz band of SND; however, the AP-SND coherence value remained high, and inhibition of SND during aortic obstruction was preserved. These data imply that non-NMDA
receptor-mediated neurotransmission in the LTF is involved in setting
the level of excitatory drive to sympathetic nerves.
D-()-2-amino-5-phosphonopentanoic
acid; caudal ventrolateral medulla; excitatory amino acid-mediated
neurotransmission; 1,2,3,4-tetrahydro-6-nitro-2,3-dioxobenzo-[f]-quinoxaline-7-sulfonamide; nucleus of the tractus solitarius; sympathetic nerve discharge
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