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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 used blockade of excitatory amino
acid (EAA) neurotransmission in the medullary lateral tegmental field
(LTF) and rostral ventrolateral medulla (RVLM) to assess the roles of
these regions in the control of inferior cardiac sympathetic nerve
discharge (SND) and mean arterial pressure (MAP) in
urethan-anesthetized, baroreceptor-denervated cats. Bilateral
microinjection of a non-N-methyl-D-aspartate (NMDA)-receptor antagonist
[1,2,3,4-tetrahydro-6-nitro-2,3-dioxobenzo-[f]quinoxaline-7-sulfonamide (NBQX)] into the LTF significantly decreased SND to 46 ± 4% of control (as demonstrated with power-density spectral analysis) and MAP
by 16 ± 6 mmHg. In contrast, bilateral microinjection of
an NMDA-receptor antagonist
[D(
)-2-amino-5-phosphonopentanoic acid
(D-AP5)] into the LTF did not decrease SND or MAP.
These results demonstrate that the LTF is an important synaptic relay in the pathway responsible for basal SND in the cat. Bilateral microinjection of NBQX or D-AP5 into the RVLM significantly
decreased power in SND to 48 ± 5 or 61 ± 5% of control,
respectively, and reduced MAP by 15 ± 2 or 8 ± 4 mmHg,
respectively. These data indicate that EAA-mediated synaptic drive to
RVLM-spinal sympathoexcitatory neurons accounts for a significant
component of their basal activity.
D()-2-amino-5-phosphonopentanoic acid; excitatory
amino acid-mediated neurotransmission; mean arterial pressure; 1,2,3,4-tetrahydro-6-nitro-2,3-dioxobenzo-[f]quinoxaline-7-sulfonamide; rostral ventrolateral medulla
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