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-induced c-Fos generation in the nucleus of
the solitary tract is blocked by NBQX and MK-801
Department of Neuroscience, The Ohio State University, Columbus, Ohio 43210
Previous studies have shown that
identified neurons of the nucleus of the solitary tract (NST) are
excited by the cytokine tumor necrosis factor-
(TNF-
). Vagal
afferent connections with the NST are predominantly glutaminergic.
Therefore, we hypothesized that TNF-
effects on NST neurons may be
via modulation of glutamate neurotransmission. The present study used
activation of the immediate early gene product c-Fos as a
marker for neuronal activation in the NST. c-Fos expression was
evaluated after microinjections of TNF-
in the presence or absence
of either the
-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonist
1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide disodium (NBQX) or the N-methyl-D- aspartate
(NMDA) antagonist MK-801. To assess the specificity of the interaction
between TNF-
and glutamate, c-Fos expression was also
evaluated after injection of oxytocin (OT) (which has a direct
excitatory effect in this area of the brain stem) in the presence and
absence of NBQX or MK-801. c-Fos labeling was significantly increased
in the NST after TNF-
exposure. Coinjection of either NBQX or MK-801
with TNF-
prevented significant c-Fos induction in the NST.
Microinjections of OT also induced significant NST c-Fos elevation, but
this expression was unaffected by coinjection of either antagonist with
OT. These data lead us to conclude that TNF-
activation of NST
neurons depends on glutamate and such an interaction is not generalized to all agonists that act on the NST.
cytokines; brain stem; dorsal vagal complex; tumor necrosis
factor-
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