Abstracts - Association for Chemoreception Sciences

conserved regions of the AOB. Here we examine the role of the
Kirrel family of transmembrane proteins in the coalescence of
VSN axons within the AOB. We find that Kirrel-2 and Kirrel-3
are differentially expressed in subpopulations of VSNs and
that their expression is regulated by activity. While Kirrel-3
expression is not required for early axonal guidance events,
such as fasciculation of the vomeronasal tract and segregation
of apical and basal VSN axons in the AOB, it is necessary for
proper coalescence of axons into glomeruli. Ablation of Kirrel-3
expression results in disorganization of the glomerular layer of
the posterior AOB and formation of fewer, larger glomeruli.
Furthermore, altered glomerular formation is associated with
loss of male-male aggression in kirrel-3 -/- mice. Taken together
our results indicate that differential expression of Kirrels on
vomeronasal axons generates a molecular code that dictates
their proper coalescence into glomeruli within the AOB.
Acknowledgements: Canadian Institutes of Health Research and
Natural Sciences and Engineering Research Council of Canada.
#P195 POSTER SESSION IV:
CHEMICAL SIGNALING AND BEHAVIOR;
ANIMAL BEHAVIOR/PSYCHOPHYSICS;
CHEMOSENSATION AND METABOLISM;
VOMERONSASAL AND CHEMICAL
COMMUNICATION
Transduction for pheromones in the main olfactory epithelium
is mediated by the Ca 2+ - activated channel TRPM5
Diego Restrepo 1 , Fabian Lopez 2 , Roberto Lopez 1 , Juan Bacigalupo 2
1
Department of Cell and Developmental Biology, Neuroscience Program
and Rocky Mountain Taste and Smell Center, University of Colorado
Anschutz Medical Campus Aurora, CO, USA, 2 Department of Biology,
University of Chile Santiago, Chile
The main olfactory epithelium contains olfactory sensory
neurons (OSNs) that respond to odorants. Interestingly, there is
growing evidence that some OSNs in this epithelium respond to
pheromones through an unknown transduction mechanism. Here
we report on a survey for pheromone transduction in a subset
of OSNs expressing the transient receptor potential channel M5
(TRPM5), a Ca 2+ -activated monovalent cation-selective channel.
As in the majority of OSNs, the cyclic nucleotide-gated (CNG)
channel subunit A2 is expressed in the cilia of OSNs expressing
GFP under control of the TRPM5 promoter. Interestingly these
TRPM5-GFP + OSNs lack the Ca 2+ -activated Cl - channel ANO2
found in the majority of OSNs. Complementary loose patch
current and Ca 2+ fluorescence recordings show that TRPM5-
GFP + OSNs respond to pheromones and not to odorants, while
TRPM5-GFP - OSNs respond to both. Finally complementary
pharmacological and TRPM5 knockout experiments show
that TRPM5-GFP OSNs respond to pheromones through the
TRPM5 channel. Thus, pheromone responses of TRPM5-GFP +
OSNs are mediated by ciliary Ca 2+ influx through CNG that
gates opening of TRPM5. Acknowledgements: Funded by NIH
DC006070 and DC004657 (D.R.), CONDECYT 1100682 (F.L.)
and CONICYT and MECESUP UCH0713 (J.B.)
#P196 POSTER SESSION IV:
CHEMICAL SIGNALING AND BEHAVIOR;
ANIMAL BEHAVIOR/PSYCHOPHYSICS;
CHEMOSENSATION AND METABOLISM;
VOMERONSASAL AND CHEMICAL
COMMUNICATION
AMYGDALAR PROCESSING OF SALIENT
CHEMOSENSORY SIGNALS
Lindsey M Biggs, Ariel R Simonton, Michael Meredith
Florida State University/Program in Neuroscience, Dept. Biol.
Sci. Tallahassee, FL, USA
Medial amygdala responds differentially to conspecific and
heterospecific chemosensory signals with different meanings
and different behavioral responses; and it may be responsible for
routing information to hypothalamic/preoptic circuits involved
in producing the appropriate responses. The vomeronasal organ
(VNO) is the primary but not only source of chemosensory
input to medial amygdala but VNO-lesions disrupt the
characteristic patterns of responses. The circuit for processing
VNO-driven chemosensory input includes the main intercalated
nucleus (mICN), one of several GABA-ir ICN cell groups
in the amygdala. mICN appears to regulate posterior medial
amygdala (MeP) activity similarly to the regulation of central
and basolateral amygdala activity by paracapsular ICN cell
groups, in the fear conditioning circuit. Using immediate-early
gene expression, we previously found that GABA-receptor-ir
cells in MeP are suppressed by heterospecific stimuli –as mICN
GABA-ir cells are activated. Now using brain slice recording
we show hyperpolarization of MeP cells by field stimulation
of local mICN. Preliminary evidence also suggests mICN
cells are suppressed by bath-applied dopamine, as is the case
for paracapsular ICN cells. The amygdala contributes to the
motivational/emotional evaluation of sensory inputs of all
modalities and for diverse behaviors. This concordance between
amygdala processing in completely different types of behavior
may indicate some commonalities in circuit organization.
Dopamine may be part of a mechanism for modulating
amygdala processing of sensory information according to brain
state or previous experience. Dopamine appears to modulate
experience-dependent chemosensory responses in basolateral
amygdala but so far we have not demonstrated an effect in
medial amygdala. Acknowledgements: Supported by NIDCD
grants R01-DC005813, T32-DC000044 and funding from Florida
State University
POSTER PRESENTATIONS
Abstracts are printed as submitted by the author(s).
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