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nerves. Results reveal that damage restricted to only one of these
nerves leads to intensified sensations mediated by undamaged
cranial nerves (increased whole mouth taste, oral touch (e.g., fats)
and oral burn/pain (e.g., chilis). In addition, retronasal olfaction is
intensified (possibly secondarily to whole mouth taste
intensification). If both nerves are damaged, these intensifications
do not occur; rather, oral sensations are reduced. Both otitis media
and tonsillectomy have been associated with intensified preferences
for high fat foods and weight gain in some individuals. Future
research will reveal how these behavioral changes are linked to the
sensory alterations produced by taste nerve damage. This may lead
to the ability to identify those individuals with histories of otitis
media or tonsillectomy that are at risk for weight gain.
Acknowledgements: We thank NIDCD for support via grants
DC000283 and DC8613.
#24
SYMPOSIUM:
CHEMICAL SENSES IN HEALTH & DISEASE
Taste Alterations in Inflammatory Disease Models
Hong Wang
Monell Chemical Senses Center Philadelphia, PA, USA
Many diseases associated with inflammation can affect taste.
For example, patients with oral and upper respiratory infections
and those with autoimmune diseases may experience taste
abnormalities of varying severity. Recent studies have shown
that numerous genes involved in immune responses are highly
expressed in taste buds. Yet, it remains largely unclear how immune
responses, such as inflammation, affect the taste system. We
recently demonstrated that in the lipopolysaccharide (LPS)-induced
acute inflammation model in mice, taste progenitor cell
proliferation and taste bud cell renewal were significantly inhibited.
The average life span of taste bud cells was shortened by LPS
treatments. Moreover, mice injected with LPS displayed a range of
altered responses to taste compounds in behavioral tests. Inhibition
of taste cell renewal was also observed in MRL/lpr mice, a model
for autoimmune diseases with chronic inflammation. The taste buds
of MRL/lpr mice were smaller than those of wild type congenic
control (MRL/+/+) mice. Immunohistochemical analyses showed a
significant reduction in the number of gustducin-positive taste
receptor cells in diseased mice. Furthermore, MRL/lpr mice
exhibited reduced responsiveness to bitter, sweet, and umami
compounds in taste behavioral tests. Together, these studies in
animal models suggest that inflammation, by affecting the renewal
and turnover of taste cells, contributes to the development of taste
disorders. Acknowledgements: Supported by NIH/NIDCD grants
DC010012 and DC011735 and NSF grant DBJ-0216310.
#25
SYMPOSIUM:
CHEMICAL SENSES IN HEALTH & DISEASE
Neuroimaging of Chemosensory Dysfunction
Claire Murphy
1,2
, Lori Haase
1,2
, Charlie D Morgan
2
, Erin Green
1,2
,
Joel Kowalewski
2
, Jessica Bartholow
2
, Roberto Zamora
2
,
John P Hegarty II
2
, Aaron Jacobson
1,2
1
San Diego State University and the University of California,
San Diego San Diego, CA, USA,
2
San Diego State University
San Diego, CA, USA
Neuroimaging is a powerful tool for investigating brain structure
and function in health and disease. We have investigated the neural
substrate of chemosensory dysfunction using EEG and both
functional and structural MRI in populations of clinical interest,
including persons at risk for Alzheimer’s disease (AD) where
olfactory impairment may signal incipient dementia. As
interventions for AD become available, determining who is at risk
and the effectiveness of interventions will be critical for initiating
treatment before significant neurological compromise. This
presentation will briefly summarize key findings and highlight new
data from ERP and fMRI studies. FMRI was conducted at 3T on a
GE scanner. Subjects performed sensory or memory tasks as brain
activation was imaged. Scans were processed with AFNI software
(Cox, 1996). Both whole brain activation and activation in regions
of interest (ROIs) were analyzed. FMRI revealed intriguing
differences between groups at risk for cognitive decline that
suggested differences in activation in key ROIs and neural
recruitment or compensation in other regions. Olfactory event-
related potentials (OERP) were recorded with Neuroscan. OERPs
demonstrated significant delays in brain response and differential
topographical distribution of the amplitude of OERPs in persons at
risk for decline, particularly in tasks that required both olfactory
function and semantic memory. Understanding the relationship
between olfactory function and the underlying substrate may
facilitate identification of biomarkers and targets for intervention to
prevent, delay or arrest disease progression in those at risk for
developing Alzheimer’s disease and in other clinical populations
with chemosensory compromise. Acknowledgements: Supported
by NIH grant #DC002064 from the National Institute on Deafness
and Other Communication Disorders and #AG004085 from the
National Institute on Aging to CM. Genotyping supported by
P50AG005131 from the National Institute on Aging to the UCSD
ADRC. We gratefully acknowledge MiRan Wang, Barbara Cerf-
Ducastel, Rick Buxton and Tom Liu.
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