Abstracts - Association for Chemoreception Sciences

olfactotoxicant satratoxin G and olfactory bulb ablation injury
was compromised in the olfactory epithelium of IP3R3 -/- mice.
The reductions in both NPY release and number of progenitor
cells in IP3R3 -/- mice point to a role of the IP3R3 in tissue
homeostasis and neuroregeneration. Collectively, these data
suggest that IP3R3 expressing microvillous cells are actively
responsive to injury and promote recovery. Acknowledgements:
Supported by NIH DC006897 (CCH), MSU institutional funds
(CCH), NIEHS T32 ES007255 (CRH), NINDS T32 NS044928
(AEP and TRI) and Swiss Fellowship for Advanced Researchers
PA 00P3_131493 (SH).
#P73 POSTER SESSION II:
OLFACTION DEVELOPMENT; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
PACAP increases [Ca 2+ ] i
in neonatal OB via direct and
indirect mechanisms
Mavis A Irwin 1 , Mary T Lucero 2
1
University of Utah Salt Lake City, UT, USA,
2
American University of the Caribbean Cupecoy, Netherlands Antilles
Our lab has been studying the pleiotropic peptide named
Pituitary Adenylate Cyclase Activating Peptide (PACAP) in
the olfactory epithelium 1 of rodents. The physiological effects
of PACAP in the olfactory bulb (OB) are still unknown.
Neonatal OB is enriched with both PACAP and its G-protein
coupled receptor PAC1R. Without PACAP, neonates often die
before weaning, suggesting that PACAP is required for normal
development. Previously, we showed that PACAP led to an
oscillating increase in [Ca 2+ ] i
in OB neurons. To address whether
the PACAP-induced responses are direct or indirect, we used
cocktails of antagonists for the GABA receptors (GABAR) and/
or glutamate receptors (GlutR) in the presence and absence of
PACAP. We performed confocal Ca 2+ imaging on live slices
from P2-P5 mice loaded with the Ca 2+ indicator dye Fluo-4
AM. The optimal dose of PACAP was empirically determined
to be 40 nM and was used in all experiments. Combined block
of GABAR and GlutR yielded a 66% decrease in numbers
of PACAP responsive cells. Blocking just GlutR resulted in
a similar reduction, suggesting that glutamate mediates the
majority of the indirect effects. Interestingly, blocking only
the GABAR resulted in block of GABA-induced initial Ca 2+
response on immature cells. However, the majority of these cells
showed the post-PACAP oscillation. Our data suggest 1) about
1/3 of the PACAP-responsive cells have direct PAC1R activity.
2) PACAP promotes glutamate release which in turn activates
2/3 of the PACAP-responsive cells. 3) GlutR may have a role in
the post-PACAP [Ca 2+ ] oscillation. 4) GABA is also released by
PACAP from PAC1R-rich GABAergic cells. In conclusion, we
find that PACAP has both direct and indirect effects on neonatal
OB neurons and may promote glutamate and GABA release in
early development. Acknowledgements: NIH 1F31DC011686-02
Blackman Trust Fund 00253 6000 16917 University of Utah
Graduate Research Fellowship 2011
#P74 POSTER SESSION II:
OLFACTION DEVELOPMENT; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
Inactivation of the Interoceptive Insula Suppresses
Chemosensory Cue Reactivity to Ethanol Following
Chronic Ethanol Exposure
Norma Castro, Emily Driver, Jason Dudley, Jessica Godfrey,
Brian Feretic, Carlo Quintanilla, Susan M. Brasser
San Diego State University/Psychology San Diego, CA, USA
Recent findings indicate that the insular cortex is critically
involved in addictive behavior to multiple drugs of abuse by
regulating an organism’s responsiveness to drug-associated
sensory cues. Damage to the insula in addicted smokers results in
a disruption of nicotine addiction, and inactivation of the insula
in rodents disrupts conditioned preference for environments
previously paired with amphetamine or nicotine. Imaging
studies have demonstrated activation in the insula during drug
craving and exposure to drug-related cues, including the taste
of alcohol in heavy drinkers. The present study measured
chemosensory responses to ethanol in chronically ethanolexposed
or naive rats under conditions of pharmacological
silencing of the visceral insula to examine the role of this brain
region in mediating responses to ethanol-associated sensory
cues. Rats were initially exposed to either a 20% ethanol
intermittent access paradigm or were given access only to water.
Following implantation of intracranial cannulae, rats from each
exposure condition were tested for brief-access lick responses
to ethanol (0-40%) after receiving bilateral insula infusions
of saline or muscimol. Alcohol-experienced rats displayed a
concentration-dependent increase in chemosensory avidity for
ethanol compared to alcohol-naive rats, evidenced by elevated
lick responses and trial sampling frequency particularly at higher
ethanol concentrations (15-40%). Inactivation of the insula
eliminated this concentration-dependent response in chronically
exposed animals, but did not modify orosensory responses to
ethanol in alcohol-naive rats. These data support insular cortex
involvement in mediating responsiveness to conditioned alcohol
chemosensory cues following chronic association of ethanol’s
taste and post-absorptive effects. Acknowledgements: Support
Contributed By: NIH AA015741
#P75 POSTER SESSION II:
OLFACTION DEVELOPMENT; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
Growth patterns of sensory neuron axon terminals in the
developing olfactory bulb
Ivan Manzini 1,2 , Thomas Hassenlklöver 1,2
1
University of Göttingen, Department of Neurophysiology and Cellular
Biophysics Göttingen, Germany, 2 University of Göttingen, DFG Cluster
of Excellence “Nanoscale Microscopy and Molecular Physiology of the
Brain” (CNMPB) Göttingen, Germany
The developing, but also the mature vertebrate olfactory
system is a site of ongoing neurogenesis. Olfactory stem cells
continuously generate new sensory neurons which extend
POSTER PRESENTATIONS
Abstracts are printed as submitted by the author(s).
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