Vol 31, Part I - forums.sou.edu • Index page - Southern Oregon ...

ABSTRACTS – Contributed Posters
LX-2 human hepatic stellate cell line to test the hypothesis
that TCDD directly affects retinol storage in hepatic stellate
cells, which store the majority of vitamin A in the human
body. LX-2 cells were treated with 5 mM retinol and 100
mM palmitic acid in the presence or absence of TCDD (10
nM). Intracellular lipid droplets were visualized 48 hr later
by staining cells with oil red O. Results indicate that TCDD
treatment abolished lipid storage in LX-2 cells. Additional
studies revealed that exposure to TCDD enhanced LX-2 cell
proliferation and increased markers of activation, such as
expression of alpha-smooth muscle actin and production of
the pro-inflammatory chemokine, monocyte chemoattractant
protein (MCP)-1. However, other activation endpoints, such
as production of collagen 1 and TGF-b1, were not altered
by TCDD treatment. Collectively, these results indicate that
TCDD treatment may directly activate hepatic stellate cells,
leading to the loss of retinol storage and the acquisition of a
pro-inflammatory phenotype. Enhanced activation of hepatic
stellate cells might explain the dysregulation of retinol
homeostasis observed in TCDD-treated rodents.
172 Stress Enhanced Fear Learning Conditioning’s Effect
on Gamma-Aminobutyric Acid Type A Receptors in the
Cortex, RAUDEL HERNANDEZ* 1 , EDWARD MEYER 2 ,
ALEXAUNDREA SMITH 2 , and IGOR SPIGELMAN 2
( 1 Howard Hughes Medical Institute Pre-College Science
Education Program; 2 UCLA School of Dentistry, 10833
Le Conte Avenue, 63-007 CHS, Los Angeles, CA 90095;
leduar7@yahoo.com).
Gamma-aminobutyric acid type A receptors
(GABA A
Rs), ion channels that control the flow of ions in the
brain, are important drug targets that are potentially altered in
response to stress. Objective: To study changes in GABA A
R
subunits (alpha1, alpha2, gamma1, gamma2 and delta) in the
cortical tissue of an animal model of stress-enhanced fear
learning (SEFL). This animal model mimics human posttraumatic
stress disorder (PTSD). Methods: SEFL rats (n=4)
were conditioned with 15 inescapable foot-shocks (1 mA,
1 second), over a period of 90 minutes. Control rats (n=4)
were not shocked, but spent the same duration of time in
the conditioning chamber. After behavioral measurements
were complete, the cortex was removed, microdissected,
homogenized and assayed for protein concentration.
The cortical tissue homogenate was then run through a
polyacrylmide gel, and transferred to a polyvinyl difluoride
(PVDF) membrane. The membranes were probed with
primary and secondary antibodies, placed into an enhanced
chemilumescent (ECL) substrate, exposed, and developed as
Western blots. This process was repeated for each specific
primary antibody for each GABA A
R subunit. Results: SEFL
rats tended to have slightly more GABA A
Rs subunits in the
cortex compared to control rats, however the difference
were not significant. Discussion: Researching the effects of
stress and anxiety on GABA A
Rs will help medical science
98
understand and potentially treat anxiety disorders like PTSD.
Conclusion: GABA A
Rs are affected by stress and anxiety,
the functional changes in the brain need to be further studied
to identify the mechanisms of how stress induces changes to
GABA A
Rs subunits in the cortex.
173 Stimulation of Adenosine A 1
Receptors in the Nucleus
Accumbens Reduces Dopamine D 1
Receptor-induced
Reinstatement by Antagonizing D 1
-mediated Enhancements
in Glutamate Transmission, BENJAMIN D HOBSON*,
CASEY E O’NEILL, and RYAN K BACHTELL
(Department of Psychology and Neuroscience and Center for
Neuroscience, University of Colorado Boulder, UCB 345,
Boulder CO 80309-0345; Benjamin.hobson@colorado.edu).
Cocaine is a psychostimulant that can lead to dependence
following continuous use, resulting in an addiction that
negatively affects the individual’s physical, mental, and
social health. The continuous potential for relapse in addicts
makes treatment of cocaine addiction especially difficult.
These studies seek to understand the neurobiological factors
contributing to relapse using a rodent model of addiction.
Stimulation of either AMPA glutamate or dopamine D 1
receptors in the nucleus accumbens (NAc) is sufficient
to induce reinstatement of cocaine seeking. Identifying
strategies to reduce the activity of these systems may provide
insight into effective treatments. Adenosine A 1
receptors
co-localize with D 1
receptors on post-synaptic terminals
of medium spiny (NAc) neurons where they counteract D 1
receptor activity through opposing intracellular signaling.
Here, we investigate the interaction between dopamine
and glutamate receptors and explore how A 1
receptor
stimulation in the NAc may reduce D 1
-induced facilitation
of AMPA receptors and cocaine seeking. Specifically,
we investigate the role of AMPA receptors in D 1
-induced
reinstatement using viral-mediated gene transfer to bidirectionally
modulate AMPA receptor activity in the NAc.
We also determined whether stimulating A 1
receptors in the
NAc would inhibit D 1
-induced reinstatement and GluA1 S845
phosphorylation using a synaptoneurosome prep and
subsequent western blot analysis. Our results demonstrate
that stimulation of A 1
receptors decreases D 1
-induced
cocaine seeking as well as GluR1 S845 phosphorylation. These
findings suggest that A 1
receptor stimulation reduces the
activity dependent AMPA receptor trafficking that drives D 1
receptor-mediated reinstatement.
174 Investigating the Interaction of Osteogenic Cell Sheets
with Osteoblast Cells, EDWIN SALVATIERRA 1 *, RAJITA
KODALI KANURU 2 , and OGAWA TAKAHIRO 2
( 1 Howard Hughes Medical Institute Pre-College Science
Education Program, UCLA School of Dentistry, 10833 Le
Conte Avenue, 63-007 CHS, Los Angeles, CA 90095; 2 The
Weintraub Center for Reconstructive Biotechnology, UCLA
School of Dentistry, 10833 Le Conte Avenue 63-014 CHS,