[Abstract Title]. - Society for Neuroscience

vago-vagal reflexes suggest that noradrenergic neurons in the NST are particularly important to
the generation of reflex gastroinhibition. Convergence of these observations led us to
hypothesize that TNF action within the NST may preferentially affect putative noradrenergic
neurons. The current study demonstrates a dose-dependent TNF activation of cells [as indicated
by cFOS production] in the NST; ~42% of these TNF-activated neurons in the NST were
phenotypically identified as tyrosine-hydroxylase (TH)-positive. In contrast, less than 10% of the
nitrergic neurons were activated after TNF exposure. To our surprise, another 45% of the cFOS
activated cells in the NST were phenotypically identified to be astrocytes. These results suggest
that TNF may work within the hindbrain to produce gastroinhibition by activating the same
phenotypic NST neurons that have been associated with driving inhibitory gastric reflexes (i.e.,
TH-positive) as well as astrocytes to, ultimately, modulate the responsiveness of NST neurons.
These observations also suggested that NST astrocytes should be activated by vagal afferent
stimulation in much the same way that NST neurons are. Indeed, calcium imaging studies show
that astrocyte activation by vagal afferent stimulation does occur.
Taken together with previous observations, the present results suggest that intense or prolonged
vagal afferent activity [induced by visceral pathway activity, the action of gut hormones or the
action of cytokines like TNF] can alter local astrocyte immediate early gene expression that, in
turn, can provoke long-term, perhaps permanent changes in the sensitivity of vagal-reflex
circuitry. Such modulation of neuronal responsiveness as a consequence glial-neuronal
communication may have precedence in migraine pathology (Thalakoti et al., 2007), enteric
celiac disease (Esposito et al., 2007), and astrocyte-neuron vulnerability to prenatal stress effects
on brain development (Barros et al., 2006). This relationship between glia and adjacent neurons
may provide another target for therapeutic intervention in autonomic disease states.
Disclosures: R.C. Rogers, None; G.E. Hermann , None.
Poster
284. Regulation of Food Intake and Body Weight: Integration of Peripheral Signals:
Systems
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 284.16/QQ11
Topic: E.07.b. Integration of peripheral signals: Systems
Title: Neural activity in rat forebrain regions induced by post-ingestive nutrients
Authors: *T. TSURUGIZAWA, T. KONDOH, A. UEMATSU, K. TORII;
Inst. Life Sci., Ajinomoto Co., Inc., Kawasaki, Japan