Basic HTML Version
#P172
POSTER SESSION IV:
CHEMICAL SIGNALING & BEHAVIOR;
PSYCHOPHYSICS; CHEMOSENSATION & DISEASE;
OLFACTION PERIPHERY; TASTE PERIPHERY
Differential Expression of TNF Receptors in Subtypes
of Taste Cells
Pu Feng, Jinghua Chai, Hong Wang
Monell Chemical Senses Center Philadelphia, PA, USA
The taste bud is a collection of a heterogeneous population of cells,
all cooperating and developing so as to maintain a homeostatic
normalcy. Aged taste cells degenerate and are replaced by young
cells differentiated from basal cells. A healthy taste system depends
on the balance of various cell types. The survival and death of cells
are tightly regulated by many factors, among which is tumor
necrosis factor (TNF). TNF plays its role by binding to its receptors
TNFR1 and TNFR2. TNFR1 contains a death domain and often
induces cell apoptosis. TNFR2, lacking a death domain, can
promote cell survival under some conditions. While our recent
studies demonstrated that taste bud cells can produce TNF, the role
of TNF in the taste system remains unclear. Indeed we even lack a
knowledge base of the expression of TNFRs in taste cells. Here we
report TNFRs expression in subtypes of taste cells in fungiform
(FF), foliate (FP), and circumvallate (CV) papillae. In FF, TNFR1
is more prevalent in type III cells than in type I and type II cells;
TNFR2 is, however, much more preferentially expressed in type I
cells. In FP, TNFR1 is moderately expressed by all three types of
cells; TNFR2 is sparse in type II cells, prevalent in type III cells,
and moderate in type I cells. In CV, TNFR1 and TNFR2 are both
more preferentially expressed in type II cells than in type I and type
III cells. This expression pattern of TNFRs strongly suggests that
TNF produced by type II taste cells (previous report) could act on
taste cells via both autocrine and paracrine mechanisms. The
differential expression levels of TNFRs in subtypes of taste cells
among the three forms of taste papillae may be related to the
different life spans of taste cells. Acknowledgements: The study
was supported by NIH/NIDCD grants DC010012 (H. W.).
#P173
POSTER SESSION IV:
CHEMICAL SIGNALING & BEHAVIOR;
PSYCHOPHYSICS; CHEMOSENSATION & DISEASE;
OLFACTION PERIPHERY; TASTE PERIPHERY
Connexin-30 and Connexin-32 Immunoreactivity in Rodent
Taste Buds
Amanda Bond
1,2
, Ruibiao Yang
1,2
, John C. Kinnamon
1,2
1
University of Denver/Department of Biological Sciences
Denver, CO, USA,
2
Rocky Mountain Taste & Smell Center
Aurora, CO, USA
Studies indicate that ATP is one of the primary neurotransmitters
in taste transduction. ATP release occurs from taste cells via
specific hemichannels, such as pannexin/connexin hemichannels
(Huang et al., 2007; Romanov et al., 2007). We hypothesize that
Type II and possibly Type III cells release ATP at sites containing
pannexin/connexin hemichannels. We have previously observed
connexin-43-LIR in a subset of Type II cells. Our recent data
indicate that connexin-30-like immunoreactivity (-LIR) and
connexin-32-LIR are also present in taste buds. Our preliminary
data suggest that connexin-30-LIR immunoreactivity is present in a
small subset of taste cells in rodent taste buds. Connexin-30-LIR
cells are spindle-shaped with large nuclei and are most likely
Type II cells. In this study, we examine the presence of connexin-
30-LIR and connexin-32-LIR in rodent taste buds through
immunocytochemical analysis and DAB immunoelectron
microscopy. We observed no colocalization of connexin-30-LIR
with 5-HT-LIR or syntaxin-1-LIR taste cells. Our preliminary data
indicate that connexin-32-LIR is present in nerve fibers. Our results
show colocalization between connexin-32-LIR and syntaxin-1-LIR
nerve processes. Thus, our results indicate that both connexin-30
and connexin-32 are present in rodent circumvallate taste buds;
however, only connexin-30 is expressed in a small subset of taste
cells while connexin-32 is present in the nerve fibers.
Acknowledgements: This work is supported by NIH grants
DC00285 and P30 DC04657
#P174
POSTER SESSION IV:
CHEMICAL SIGNALING & BEHAVIOR;
PSYCHOPHYSICS; CHEMOSENSATION & DISEASE;
OLFACTION PERIPHERY; TASTE PERIPHERY
Glutamate Elicits Inhibition in Mouse Taste Buds
Yijen A. Huang
1
, Jeff Grant
1
, Stephen D. Roper
1,2
1
Department of Physiology & Biophysics, Miller School of
Medicine, University of Miami Miami, FL, USA,
2
Program in
Neuroscience, Miller School of Medicine, University of Miami
Miami, FL, USA
Gustatory afferent fibers innervating taste buds store
neurotransmitters such as glutamate, but little is known about the
function of these transmitters. Recent studies suggest that glutamate
may be an efferent transmitter (Vandenbeuch et al., 2010; Huang et
al., 2012). However, to date, the effect of glutamate on signal
processing in taste buds is not well understood. In this study, we
characterized ionotropic synaptic glutamate receptors present on
taste cells. These receptors appear to underlie the postulated
efferent transmission. Specifically, we loaded mouse vallate taste
cells with Fura 2 and tested their responses to a low (synaptic)
concentration of glutamate (100 μM). We also measured taste-
evoked transmitter (ATP) release from taste buds and taste cells.
The findings are that a significant fraction of Presynaptic (Type III)
taste bud cells (~50%) respond to glutamate, but that only few
Receptor (Type II) taste cells (4%) are activated by this
transmitter. Presynaptic cells were also stimulated by NMDA
(100 μM) and kainic acid (KA, 100 μM). At these concentrations
and with these compounds, glutamate, NMDA, and KA activate
ionotropic glutamatergic synaptic receptors, not glutamate taste
(umami) receptors. Consistent with these results, applying
glutamate, NMDA, or KA caused taste buds to secrete 5-HT, a
Presynaptic taste cell transmitter. Importantly, glutamate-evoked 5-
HT release inhibited Receptor (Type II) cells and reduced their
ability to secrete transmitter (ATP). We conclude that the net effect
of glutamate as an efferent transmitter in taste buds is inhibitory—
i.e., glutamate acts via serotonergic mechanisms to reduce taste-
evoked transmitter release. Acknowledgements: 5R01DC007630
Abstracts | 85
Abstracts are printed as submitted by the author(s)
P O S T E R P R E S E N T AT I O N S