Abstracts - Association for Chemoreception Sciences

#P70 POSTER SESSION II:
OLFACTION DEVELOPMENT; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
Effect of kamikihito (TJ-137) on nerve growth factor and
olfactory nerve in vivo
Junpei Yamamoto 1 , HIdeaki Shiga 1 , Kohshin Washiyama 2 ,
Ryohei Amano 2 , Takaki MIwa 1
1
Otorhinolaryngology, Kanazawa Medical University Ishikawa, Japan,
2
Quantum medical technology, Kanazawa University Ishikawa, Japan
Background: A Kampo product, kamikihito (product name code:
TJ-137), has ingredients that promote nerve growth. Paclitaxel,
a cancer chemotherapeutic agent, is toxic to olfactory nerve cells
in vivo. To show TJ-137 pre-medication effect on nerve growth
factor (NGF) in olfactory bulb and paclitaxel induced olfactory
neuropathy in vivo. Methods: Female 7-week-old Bulb/c mice
were fed food containing TJ-137, or control food, for 14 days
before and after intravenous paclitaxel administration. NGF
was assessed with ELISA in the olfactory bulb of mice fed
food containing TJ-137 (n=9), or control food (n=9) for 14
days. The epithelial changes in the nasal turbinates of mice
were assessed by H&E and immunohistochemical staining for
the olfactory marker protein (OMP). The accumulation of the
neuronal tracer (Dextran tetramethylrhodamine) in the olfactory
bulb was assessed in frozen sections of mice 48 h after nasal
administration of the tracer. Results: NGF was significantly
increased in the olfactory bulb of mice fed food-containing
TJ-137 than in the control mice (P=0.017). The epithelium
of nasal turbinates of TJ-137 treated mice was less injured
than that of the control mice after paclitaxel administration.
The accumulation of the neuronal tracer in the olfactory bulb
was higher in the TJ-137 treated mice compared to controls.
Conclusion: We found that TJ-137 is effective in increasing
NGF in olfactory bulb and reducing paclitaxel induced olfactory
neuropathy in vivo. Acknowledgements: Assist Kaken from
Kanazawa Medical University (2012)
#P71 POSTER SESSION II:
OLFACTION DEVELOPMENT; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
Fgf8 Defines Neurogenic Vomeronasal and GnRH Neurogenic
Mileu by Influencing BMP and BMP Antagonists Expression.
Paolo E. Forni 1 , Kapil Bharti 2 , Susan Wray 1
1
National Institute of Neurological Disorders and Stroke/NIH
Bethesda, MD, USA, 2 National Eye Institute/NIH Bethesda,
MD, USA
FGF8 plays a pivotal role in development of craniofacial
structures, the olfactory/vomeronasal system and GnRH
neurons. BMPs can antagonize FGFs expression and signal,
BMP and FGF8 signaling are known to exert opposite roles
in defining epithelial versus neurogenic fate. We analyzed
the relation between Fgf8, BMP and BMP anatgonists in the
developing olfactory pit in two Fgf8 hypomorph mouse models,
expressing different levels of FGF8. In both mutant mouse
models, Fgf8 neo/neo and Fgf8 neo/Null , regardless of the FGF8
dosage, overlapping defects were observed in the olfactory pit:
lack of neurons formation limited to the ventral area of the
developing nasal pit and the proximal portion of respiratory
epithelium, where GnRH neurons normally form. Analyzing
expression of BMP4 and BMP antagonist Noggin we found
a previously not described large mesenchymal Noggin source
that sharply defines a BMP free GnRH and VNO neurogenic
border. In Fgf8 hypomorphs BMP4 and Noggin expression were
found to be altered, with Noggin no longer defining the GnRH
and VNO neurogenic border. These data suggest that the role
played by FGF8 in controlling cell fate specification and neural
patterning of the olfactory pit is in large part indirect as Fgf8
levels affect both BMP and Noggin expression in the pit and
nasal mesenchyme. BMP and Noggin expression respectively
define the epithelial or neurogenic permissive borders. The
previously described lack of GnRH neuron specification in
animals with chronically reduced FGF8 reflects the loss of a
large neurogenic permissive milieu that includes the entire VNO.
Acknowledgements: The work presented was supported by
the Intramural Research Program of the National Institutes of
Health, National Institute of Neurological Disorders and Stroke
#P72 POSTER SESSION II:
OLFACTION DEVELOPMENT; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
An IP3R3- and NPY-expressing microvillous cell mediates
tissue homeostasis and regeneration
Colleen C. Hegg 1,2,3 , Cuihong Jia 1 , Sebastien Hayoz 1 ,
Chelsea R. Hutch 2,3 , Apryl E. Pooley 2 , Tania R. Iqbal 2
1
Michigan State University Pharmacology and Toxicology East Lansing,
MI, USA, 2 Neuroscience Program East Lansing, MI, USA,
3
Center for Integrative Toxicology East Lansing, MI, USA
Calcium-dependent release of neurotrophic factors plays an
important role in the maintenance of neurons, yet the release
mechanisms are understudied. The inositol triphosphate (IP3)
receptor is a calcium release channel that has a physiological
role in development, sensory perception, neuronal signaling and
secretion. In the olfactory system, the IP3 receptor subtype 3
(IP3R3) is expressed exclusively in a microvillous cell subtype
that is the predominant cell that expresses neurotrophic factor
neuropeptide Y (NPY). We hypothesized that the IP3R3-
expressing microvillous cells secrete sufficient NPY needed for
both the continual maintenance of the neuronal population
and for neuroregeneration following injury. We addressed this
question by assessing the release of neurotrophic factor NPY
and regenerative capabilities in wild type mice, IP3R3 +/- , and
IP3R3 -/- mice. Injury, simulated using extracellular ATP as a
model, induced IP3 receptor-mediated NPY release in wild-type
mice. ATP-evoked NPY release was impaired in IP3R3 -/- mice,
suggesting that IP3R3 contributes to NPY release following
injury. Under normal physiological conditions, both IP3R3 -
/-
mice and explants from these mice had fewer progenitor
cells that proliferate and differentiate into immature neurons.
Although the number of mature neurons and the in vivo rate of
proliferation were not altered, the proliferative response to the
POSTER PRESENTATIONS
Abstracts are printed as submitted by the author(s).
56