Abstracts - Association for Chemoreception Sciences

#46 PLATFORM PRESENTATIONS: TASTE
Phenotypic Characterization of a Caudal to Rostral
Intrasolitary Pathway
Joseph M Breza, Zhixiong Chen, Joseph B Travers, Susan P Travers
The Ohio State University Columbus, OH, USA
Interactions between gustatory and visceral signals modulate
ingestive behavior. The current study explored such interactions
in the nucleus of the solitary tract (NST) where gustatory and
visceral primary afferents terminate in largely separate rostral
(rNST) and caudal (cNST) regions, respectively. Previous
anterograde tracing suggests an intrasolitary projection from
cNST to rNST (Karimnamazi et al.,’98) but the phenotypes
of these connections have not been characterized. We made
electrophysiologically–guided iontophoretic injections of the
retrograde tracer, Fluoro-Gold (FG), into gustatory NST in wildtype
and transgenic mice expressing EGFP under the control
of the GAD67 promoter. Sections were immunostained for FG
and tyrosine hydroxylase (TH) to identify catecholaminergic
neurons or PHOX2b, a transcription factor that colocalizes with
a subset of glutamatergic cells. Retrogradely–labeled cNST
neurons extended caudal to obex. At a mid–postremal level,
where several neuron types, including A2 catecholaminergic cells
important in satiety are prominent, the intrasolitary pathway
contained both PHOX2b/excitatory (~65+2.7%) and GAD67/
inhibitory (27+2.5%) projections, with PHOX2b neurons
located preferentially in the medial and intermediate NST and
the GAD67 neurons distributed more laterally, including the
ventral lateral NST. A smaller population (7+1.2%), presumably
a subset of the PHOX2b cells, was double-labeled for FG and
TH. Parallel experiments in rats showed a similar distribution of
FG neurons labeled with dopamine beta hydroxylase implying
that most TH–labeled neurons in mice are noradrenergic.
In addition, in vitro recordings from rNST demonstrate that
norepinephrine has a suppressive effect on solitary tract–evoked
responses, suggesting a functional role for the A2 projection.
Acknowledgements: Supported by DC00416 & T32DE014320
#47 PLATFORM PRESENTATIONS: TASTE
Longitudinal analysis of 40% calorie restriction on rat taste
bud morphology and expression of sweet taste modulators
Huan Cai, Wei-na Cong, Rui Wang, Caitlin Daimon, Patrick Chirdon,
Rafael deCabo, Stuart Maudsley, Bronwen Martin
National Institute on Aging Baltimore, MD, USA
Taste perception is strongly associated with body weight and
metabolic state. Caloric restriction (CR) is a well-characterized
intervention that reduces body weight and improves metabolic
function. In this study, we performed a longitudinal analysis to
determine the effects of 40% CR on rat taste bud morphology
and expression of sweet taste modulators. Immunohistochemical
analyses of the effects of 40% CR on taste buds were made with
5-, 17- and 30-month old male Fisher 344 rats. No significant
effects of 40% CR on taste bud size and number of taste cells
per taste bud were noted. However, 30-month old rats (both
ad libitum (AL) and calorie restriction (CR) groups) possessed
smaller taste bud size and fewer taste cells per bud than
5- (significant) or 17- (non-significant) month old CR or AL
rats. There was no significant effect of 40% CR or aging on
Type 1 (NTPDase 2), Type 2 (PLC-beta 2), or Type 3 (NCAM)
taste cells marker expression. In contrast, both 40% CR and
AL 30-month old rats demonstrated significantly lower Type 4
(Shh) taste cell marker expression. We found that a-gustducin
expression was significantly higher in 5-month old 40% CR rats
compared to AL, with similar trends for T1r3 and glucagonlike
peptide 1 (GLP-1) expression. However, T1r3, GLP-1 and
a-gustducin expression were decreased in 30-month old 40%
CR rats compared to age-matched AL rats. Leptin receptor
expression was significantly higher in 17- and 30-month old 40%
CR rats, compared to age-matched AL rats. Our findings suggest
that short- and long-term CR elicit differential responses on rat
taste bud morphology and sweet taste modulator expression.
This is likely due to long- and short-term calorie intake
and metabolic homeostatic adaptations to the CR regimen.
Acknowledgements: This work was supported entirely by the
Intramural Research Program of the National Institute on
Aging, National Institutes of Health.
#48 SYMPOSIUM:
EXPERIENCE DRIVEN PLASTICITY
OF THE OLFACTORY SYSTEM
Experience Driven Plasticity of the Olfactory System
Xavier Grosmaitre
CSGA, UMR 6265 CNRS - 1324 INRA - Université de Bourgogne
Dijon, France
The olfactory system has been thoroughly investigated during
several decades. A number of its functions have been well
described such as i) the olfactory transduction pathways; ii) the
central odor processing and cerebral and neural networks; iii)
the mechanisms of neurogenesis and synaptic plasticity. The
olfactory system reveals itself as a flexible sensory processing
system. While the implication of experience and internal state
on olfactory detection and processing has been explored, some
points remain unclear: whether experience can modulate specific
populations of olfactory sensory neurons (OSNs) and olfactory
bulb (OB) input and output maps. New tools were recently
developed to analyze the plasticity of the olfactory system such
as genetic labeling of specific population of OSNs (i.e. expressing
specific OR), molecular biology tools (qRT-PCR), genetic
labeling for synaptic transmission imaging and in vivo imaging.
This symposium focuses on the dynamic nature of olfactory
processing: the effects of experience on how odors are processed
from olfactory sensory neurons to higher-order structures and
how recent techniques are used to investigate these questions in
different structures and models. In mice, we will discuss: i) the
effects of olfactory experience on specific OSNs populations and
synaptic transmission; ii) the effects of emotional experience
on OSNs function; ii) the importance of the balance between
activity, regeneration and remodeling for OB plasticity; iii) the
use of long-term imaging of odor representations in awake mice
to explore olfactory plasticity. Finally, plasticity induced by
ORAL ABSTRACTS
Abstracts are printed as submitted by the author(s).
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