olfactory ensheathing glia, also exhibited a graded expression of
injury markers including activated caspase-3, Beta-APP and
p75NTR, with ipsilateral showing higher levels than contralateral
and both significantly higher than sham. At a behavioral level we
also found that this injury results in a clear loss of olfactory
function. We demonstrate that following a brief 30 day recovery
period there is partial restoration of neural circuitry and olfactory
function. Together these data establish the mouse olfactory system
as a new model to study TBI, serving as a platform to understand
neural disruption and the potential for circuit restoration.
Acknowledgements: Henry M. Jackson Foundation/The Center for
Neuroscience and Regenerative Medicine
#P101
POSTER SESSION III:
OLFACTION DEVELOPMENT & CNS;
HUMAN PSYCHOPHYSICS; TASTE PERIPHERY
Increased sensitivity and decreased selectivity to odorants in
controlled cortical impact mice
Zhishang Zhou
1,2
, Elizabeth Steuer
1,2
, Leonardo Belluscio
1,2
1
National Institute of Neurological Disorders and
Stroke/Developmental Neural Plasticity Section Bethesda, MD,
USA,
2
Henry Jackson Foundation/Center for Neuroscience and
Regenerative Medicine Bethesda, MD, USA
Olfactory dysfunction is an early indicator of traumatic brain injury
(TBI) with patients often reporting a loss of olfactory function.
Using controlled cortical impact (CCI) to the anterior cortex as a
TBI model, we studied the olfactory responses in the olfactory bulb
(OB) using the UBI7 transgenic mouse line. In these mice, all the
olfactory sensory neurons (OSNs) express low levels of the I7
receptor in addition to their endogenous receptors. Using multi-
electrode recordings we detected and compared OB responses to
Octanal, an I7 receptor ligand, in both CCI and control mice.
Here we report clear and reliable odor-induced activation of the
OB in all the experiments. Interestingly, we reveal that the CCI
mice show activation at lower Octanal concentrations and greater
prolonged activity compared to control mice, suggesting increased
odor sensitivity in CCI mice. We tested additional odors,
Acetophenone, Amyl-acetate, Butanal and Propanal, and again
found that CCI mice exhibited higher probability of activation than
controls consistent with an increased sensitivity and decreased
selectivity in odor responses. Finally, we used a buried-food
behavioral assay and showed that CCI mice could indeed locate
food faster than controls supporting an enhancement in olfactory
sensitivity. As TBI has mild, moderate and severe types, we
propose that the olfactory system may provide a new means to
distinguish between different TBI types and study their
mechanisms. Acknowledgements: Intramural funding from
NINDS. Funding from Henry Jackson Foundation.
#P102
POSTER SESSION III:
OLFACTION DEVELOPMENT & CNS;
HUMAN PSYCHOPHYSICS; TASTE PERIPHERY
Blocking the lateral olfactory tract
in vivo
alters spontaneous
activity in the main olfactory bulb of the rat
Neil C. Ford, Edwin R. Griff
University of Cincinnati, Department of Biological Sciences
Cincinnati, OH, USA
The lateral olfactory tract (LOT) contains the axons of mitral
and tufted cells as well as centrifugal fibers that terminate in the
main olfactory bulb (MOB). This study evaluated the effect of
blocking axon conduction in the LOT by topically applying 2%
lidocaine with a small ball of cotton. LOT blockade was assessed
by recording field potentials (fp’s) in the MOB evoked by
stimulating LOT caudal to the block. Direct effects of lidocaine on
the bulb were assessed by recording fp’s evoked by stimulating
LOT rostral to the block and/or by stimulating the olfactory
nerve. The mean spontaneous activity (SA) of single units was
recorded in each layer (Glomerular Layer (GL), External Plexiform
Layer (EPL), Mitral Cell Layer (MCL), Granule Cell Layer (GCL))
before and after lidocaine application. Each site of single unit
recording of SA in each layer of the MOB was confirmed by a dye
spot. Overall, there was no change in the mean rate (paired t-test:
0.89 ± 11.2 Hz, p=0.6); however, there was considerable variability.
In the GL, 6 units decreased in activity by a mean of 54.2 ± 27.7%
and 7 units did not change. In the EPL, 4 units decreased in activity
by a mean of 49.2 ± 32.2%, 2 increased by 32.7 ± 18.3% and 6 did
not change. In the MCL, 7 units decreased in activity by a mean of
69.3 ± 18.8%, 8 increased by 43.4 ± 13.7% and 2 did not
change. In the GCL, 3 units decreased in activity by a mean of
51.9 ± 25.3%, 2 increased by 33.6 ± 18.4% and 5 did not
change. We conclude that tonic release of excitatory and/or
inhibitory signals from centrifugal inputs to the MOB modulates
spontaneous activity of many bulbar neurons. Ongoing experiments
will attempt to determine the specific source(s) of this input and
the bulbar circuits that are affected. Acknowledgements: University
of Cincinnati Research Council
#P103 WITHDRAWN
#P104
POSTER SESSION III:
OLFACTION DEVELOPMENT & CNS;
HUMAN PSYCHOPHYSICS; TASTE PERIPHERY
PAC1R is Present and Functional before the Maturation
of Granule Cells in Mouse Olfactory Bulb
Mavis A Irwin, Lucero T Mary
Department of Physiology Salt Lake City, UT, USA
The GABAergic granule cells (GC) in the olfactory bulb (OB)
develop from Dlx2 expressing neuroblasts derived from stem cells
within the subventricular zone (SVZ). The neuroblasts migrate to
the OB and enter the granule cell layer (GCL). From there, the
neuroblasts either stop migrating and become immature neurons or
continue migrating to the glomerular layer of the OB. The
successful migration of neuroblasts from the SVZ to the GCL is a
critical component of postnatal OB development. Pituitary
Adenylate Cyclase-Activating Polypeptide (PACAP) and its
G-protein coupled receptor (PAC1R) are involved in modulating
the Ca
2+
activity of developing OB neurons
1
. Ca
2+
activity in the
CNS is thought to be critical for the establishment and survival of
Abstracts | 61
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