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22 | AChemS Abstracts 2012
Abstracts are printed as submitted by the author(s)
#40
SYMPOSIUM: WIRING NEURAL CIRCUITS
IN OLFACTORY SYSTEMS
Tracing Innate and Adaptive Olfactory Circuits in
the Fly Brain
Vanessa Ruta
The Rockefeller University New York, NY, USA
Certain odors induce stereotyped instinctive behaviors suggesting
that they activate genetically specified neural circuits. However,
the vast majority of odors have no inherent valence to an individual
but only acquire behavioral significance through associations
formed in the context of experience. How is olfactory information
differentially processed in the brain to support these instinctive or
adaptive behaviors? We are addressing this question in the fruit fly,
Drosophila melanogaster,
an insect that exhibits a rich repertoire of
odor-driven behaviors mediated by a relatively simple olfactory
system with an analogous architecture to that in mammals.
Interestingly, in the fly brain olfactory signals are transmitted in
parallel to two discrete higher brain centers, the mushroom body
and the lateral horn, that mediate learned and innate olfactory
behaviors. We have devised novel neural tracing approaches using
photoconvertible fluorophores, precise electroporation of diffusible
dyes and single cell electrophysiology to reveal the functional
organization of olfactory pathways in the lateral horn and
mushroom body. We will describe our recent data identifying
differences and commonalities in the wiring of these higher
brain centers.
#41
PLATFORM PRESENTATIONS:
TASTE
Shh-expressing basal cells are immediate precursors of taste
receptor cells
Linda A. Barlow
1
, Jennifer K. Scott
1
, Hirohito Miura
2
1
Department of Cell & Developmental Biology-Rocky Mountain
Taste & Smell Center, University of Colorado Denver, School of
Medicine Aurora, CO, USA,
2
Dept of Oral Physiology, Kagoshima
University Graduate School of Medical and Dental Sciences
Kagoshima, Japan
Taste buds are aggregates of modified epithelial cells that transduce
gustatory stimuli into electrochemical signals which are transmitted
to the brain. In addition to this neuron-like function, taste cells
retain the epithelial characteristic of continuous turnover
throughout adult life. The current model of taste bud regeneration
holds that taste progenitors reside outside of buds; these cells
divide to produce daughters, which exit the cell cycle, enter buds as
postmitotic precursors, and differentiate into 1 of 3 types of taste
cells. In addition to these 3 fusiform types, taste buds house a set of
basal cells, many of which express the morphogen, Sonic hedgehog
(Shh). Previously, Miura et al. (2006) showed that Shh+ cells are
postmitotic, and proposed that Shh+ basal cells are immediate
precursors for taste receptor cells. To test this hypothesis, we used
molecular genetic cell labeling to track the fate of Shh+ basal cells
in taste buds of adult mice. Specifically, ShhCre
ER
;R26RLacZ mice
were treated with tamoxifen, daily or every other day, for 4, 8, or
16 days to drive Cre activation and thus beta-gal expression in
Shh+ cells. In taste tissue from these mice examined at 1, 7 or 10
days after the final tamoxifen dose, we found Shh+ cells had
differentiated into fusiform taste cells, including both types II and
III, as assessed via specific immunomarkers. We also encountered
beta-gal+ cells with complex morphology where they appeared to
wrap other taste cells, consistent with type I identity. Importantly,
we found that Shh+ descendent cells occurred singly in taste buds,
rather than in pairs, consistent with the observation that Shh+
cells are postmitotic. Thus, we show that Shh+ basal cells are
postmitotic precursors that differentiate directly into each of the
3 functional taste cell types. Acknowledgements: Supported by
NIH/NIDCD R01 DC008373 and ARRA DC008373-03S1 to
LAB, and the Rocky Mountain Taste & Smell Center, P30
DC003947 to D. Restrepo.
#42
PLATFORM PRESENTATIONS:
TASTE
Sweet taste responses are enhanced by adenosine acting
through A2B receptors
Robin Dando
1
, Gennady Dvoryanchikov
1
, Elizabeth Pereira
1
,
Nirupa Chaudhari
1,2
, Stephen D Roper
1,2
1
University of Miami Miller School of Medicine, Department
of Physiology and Biophysics Miami, FL, USA,
2
University of
Miami Miller School of Medicine, Program in Neuroscience
Miami, FL, USA
Mammalian taste cells are susceptible to modulation by a number
of circulating factors. Some of these factors affect the transduction
of a single taste quality. Examples include leptin which selectively
affects sweet taste (Kawai et al, 2000), or insulin, which affects salt
taste (Baquero & Gilbertson, 2011). Here, we show that adenosine
is another such modulator, specific for sweet taste. ATP is released
from taste cells upon detection of sweet, bitter or umami
compounds. Because the enzymatic machinery to degrade ATP to
AMP is present in abundance in taste buds, we reasoned that AMP
might be further degraded to adenosine. Indeed, we found that both
the ecto-nucleotidase NT5E, and to a lesser extent prostatic acid
phosphatase (ACPP), are present in taste buds, primarily on
Type III (Presynaptic) cells. This suggests that adenosine is
present in significant quantities in taste buds. Adenosine is a
powerful neuromodulator in the nervous system, acting on both
excitatory and inhibitory receptors. Using RT-PCR on single taste
cells, we demonstrated that the excitatory A2B receptor is
predominantly expressed in cells expressing T1R sweet
receptors. In taste cells, Ca
2+
mobilization evoked by artificial
sweeteners was significantly enhanced by adenosine
(50 μM). Furthermore, by using biosensor cells, we found that
sweet-evoked ATP release from Type II (Receptor) cells was
greatly amplified by adenosine (5 μM). Blocking A2B receptors
with MRS 1706 (250 nM) significantly reduced sweet-evoked
ATP release, indicating that adenosine modulation is intrinsic to
taste buds. Bitter or umami tastes were unaffected. The findings
demonstrate that adenosine, formed during taste stimulation by the
degradation of ATP, exerts positive feedback selectively on sweet
responses. Acknowledgements: This research was supported by
NIH Grants 2R01DC007630 and 5R01DC000374 to S.D.R. and
R01DC006021 and R01DC006308 to N.C.
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