Abstracts - Association for Chemoreception Sciences

#P108 POSTER SESSION II:
OLFACTION DEVELOPMENT; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
#P109 POSTER SESSION II:
OLFACTION DEVELOPMENT; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
Dynamics of reward-mediated neural plasticity in honey
bee antennal lobe glomerulus
Adrian Smith 1,4 , Irina Sinakevitch 1 , Ramon Huerta 2 ,
Maxim Bazhenov 3 , Brian H Smith 1
1
Arizona State University, School of Life Science, Tempe, AZ, USA,
2
BioCircuits Institute, University of California San Diego, La Jolla,
CA, USA, 3 Department of Cell Biology and Neuroscience, University
of California, Riverside, CA, USA, 4 Arizona State University,
Mathematical, Computational and Modeling Sciences Center, Applied
Mathematics for the Life and Social Sciences Tempe, AZ, USA
Recent studies of neural plasticity in the honey bee antennal lobe
(AL) show the response dynamics of uniglomerular projection
neurons (uPNs) to an odor change after association of that odor
with sucrose reinforcement. The octopamine (OA), released by
the ventral unpaired median neuron (VUM), is necessary for
these neural plasticity changes. Using anti-OA staining, we found
that the varicosity-like distributions of VUM branch mostly in
the cortex of the glomerulus, where it potentially modulates
olfactory receptor neurons (ORNs), local interneurons (LNs)
and uPNs. We develop a biophysical model of the AL circuit
to investigate modulatory mechanisms that can explain existing
data on the dynamical changes of uPNs during associative
learning, and lead to insights for new experiments. First, we
hypothesize that OA release from VUM varicosities would be
dependent on correlated firing between ORNs and VUM during
associative learning. This mechanism implies simultaneous
cholinergic and octopaminergic transmission to PNs. Second,
OA release from VUM acts on AmOA1 receptors expressed
in LNs. AmOA1 activation increases the excitability of LNs,
leading to increased inhibition of PNs. Third, release of OA
leads to direct activation of beta-adrenergic-like OA receptors.
This increases the levels of cAMP, triggering PKA-dependent
translation and upregulation of alpha7 nicotinic acetylcholine
receptor (nAChR) subtypes. nAChR-dependent Ca2+ influx
triggers transcription factors that upregulate transient Shal-type
K+ channels, preventing excessive membrane depolarization.
Based on these hypotheses, we propose the model to characterize
dynamics of the uPN as a function of the relative expression
of Shal-type K+ channels and OA release. Acknowledgements:
NIH-NCRR RR014166 and NIH grant R01 DC011422
In vivo imaging of odor-evoked responses in the mouse
olfactory bulb using the FP voltage sensor ArcLight and the
calcium sensor GCaMP3
Douglas A Storace 1 , Lawrence B Cohen 1, 2 , Uhna Sung 2
1
Yale University / Department of Cellular and Molecular Physiology
New Haven, CT, USA, 2 Korea Institute of Science and Technology /
Center for Functional Connectomics Seoul, South Korea
Optogenetic reporters of membrane potential allow for recording
of genetically distinct populations of neurons, although their
usefulness to date has been limited by poor in vivo expression,
small signal sizes and slow kinetics. The fluorescent protein (FP)
voltage sensor ArcLight exhibits a change in fluorescence to a
100 mV depolarization five times larger than previously reported
probes in HEK 293 cells. However, recordings of ArcLight in
mammalian neurons have been limited to cultured neurons. The
goal of the present study was to examine ArcLight responses in
the olfactory bulb in an in vivo preparation, and compare them
to those of the genetically encoded calcium indicator GCaMP3.
AAV-1 viral transduction was used to express ArcLight and
GCaMP3 in the mouse olfactory bulb. Odors were presented at
different stimulus duration and concentrations, and the resulting
patterns of activation were imaged. Odor-specific patterns of
activation were obtained from both ArcLight and GCaMP3,
although only ArcLight had sufficiently fast temporal kinetics
to clearly detect population activity elicited by individual sniffs
to an odor. The results indicate that ArcLight can be used as a
reliable detector of odor-evoked population signals in the mouse
olfactory bulb. Acknowledgements: Supported by US NIH
Grants DC005259 and NS057631, Grant WCI 2009-003 from
the National Research Foundation of Korea, and an
James Hudson Brown – Alexander Brown Coxe Fellowship
from Yale University.
#P110 POSTER SESSION II:
OLFACTION DEVELOPMENT; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
Expression and Activity of Glucagon-like Peptide-1 in the
Mouse Olfactory Bulb
Nicolas Thiebaud 1 , Ida Llewellyn-Smith 2 , Fiona Gribble 3 , Frank
Reimann 3 , Stefan Trapp 4 , Debra A. Fadool 5
1
The Florida State University, Department of Biological Science
Tallahassee, FL, USA, 2 Flinders University, Centre for Neuroscience
Bedford Park, Australia, 3 Addenbrooke’s Hospital, Cambridge Institute
for Medical Research Cambridge, United Kingdom, 4 Imperial College
London, Department of Surgery and Cancer London, United Kingdom,
5
The Florida State University, Program in Neuroscience and Molecular
Biophysics Tallahassee, FL, USA
POSTER PRESENTATIONS
A number of peptides and hormones that are known to regulate
energy metabolism or feeding behavior have been identified in
the olfactory system. These hormones are thought to modulate
olfactory perception and function to suppress or promote
Abstracts are printed as submitted by the author(s).
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