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or saline vehicle. Injured parietal cortex and underlying hippocampus
were probed via western blotting on post-injury day (PID) 2, 4, and 14.
We examined various markers of NMDAR mediated plasticity, including
NR2A, NR2B, NR1, CaMKII, pCaMKII, CREB, and pCREB. This study
is novel in charting the time-course of plasticity-related molecular
changes after injury and with glutamatergic treatment. We found that
reductions in NR2A (16% reduction in untreated injured vs. uninjured,
p < 0.1) and pCaMKII (39% reduction in untreated injured vs. uninjured,
p < 0.05) in the injured rat hippocampus on PID4 were alleviated fol-
lowing treatment with DCS. Further, NR2A expression in injured PID4
hippocampus was significantly higher in treated injured animals than in
untreated injured animals at the p < 0.1 level. Injured rats treated with
DCS have similar levels of NMDAR relatedmolecular markers compared
to uninjured, untreated controls (there were no significant differences
between treated injured animals and controls in NMDAR related mo-
lecular expression). Early DCS treatment helps to alleviate some early
deficits in NMDAR related signaling in injured hippocampus following
severe lateral fluid percussive injury. Thus, DCS administration following
pediatric TBI in the subacute phase represents a powerful potential target
for early intervention. This research was supported by UCLA BIRC,
NS027544, HD076418, and the Joseph Drown Foundation.
Keywords: Pediatric, D-Cycloserine, NMDAR, FPI, Severe FPI
A8-08
MIASCI ONLINE: AN ANNOTATION TOOL FOR THE MINI-
MAL INFORMATION ABOUT A SPINAL CORD INJURY EX-
PERIMENT (MIASCI) REPORTING STANDARD
Vance Lemmon1,3, Alison Callahan2, Deepthi Puram3, Julio Perez
Baez3, Saminda Abeyruwan4,3, Adam Ferguson5, Phillip Popovixh6,
John Bixby1,3
1Univ. of Miami, Miami Project for Cure Paralysis, Miami, USA
2Stanford Univ., Stanford Center for Biomedical Informatics Re-
search, Stanford, USA
3Univ. of Miami, Center for Computational Science, Coral Gables, USA
4Univ. of Miami, Department of Computer Science, Coral Gables, USA
5Univ. of Calif, San Francisco, Brain and Spinal Injury Center (BA-
SIC), Department of Neurological Surgery, San Francisco, USA
6The Ohio State Univ., Center for Brain and Spinal Cord Repair and
the Department of Neuroscience, Columbus, USA
The lack of reproducibility in many areas of science, including spinal
cord injury (SCI) research, results in increased operational costs and a
decline in the productivity of research and development. Poor repro-
ducibility is due in part to the lack of common reporting standards. To
address this significant problem, over the past four years an ad hoc
consortium of scientists has developed a minimal information reporting
standard for SCI experiments, known as MIASCI. Our latest version of
MIASCI captures information about 11 aspects of an SCI experiment:
investigator, organism, surgery, perturbagen, cell transplantation, bio-
materials, histology, immunohistochemistry, imaging, behavior, bio-
chemistry, molecular biology, and data analysis and statistics. For each
of these aspects, MIASCI enables scientists to capture essential meta-
data about the study design, materials and methods. Collecting all the
information needed to comply with MIASCI is challenging and if an
entirely manual entry approach is used, it is difficult to describe ex-
perimental workflows or study groups, and the relationships between
them. Here, we present MIASCI Online, a web-based annotation tool
that makes use of existing ontologies and addresses these problems.
Importantly, MIASCI Online produces output that is both human
readable and ready for deposit and analysis in data- and knowledge-
bases. Example queries supported by MIASCI Online will be illustrated
and their role in facilitating scientific discovery discussed.
Acknowledgments
Supported by NINDS NS080145 and NICHD HD057632
Keywords: ontology, database, reporting standard, informatics, re-
producibility
A8-09
IMMEDIATE AND PERSISTENT DENDRITIC HYPER-
TROPHY IN THE BASOLATERAL AMYGDALA FOLLOWING
EXPERIMENTAL DIFFUSE TRAUMATIC BRAIN INJURY
Ann Hoffman1,2, Pooja Paode2, J. Bryce Ortiz 2, Salma Kemmou2,
Hazel May3, Cheryl Conrad2, Jonathan Lifshitz2,3,4, Theresa Currier
Thomas3,4
1UCLA, Neurosurgery and Psychology, Los Angeles, USA
2Arizona State University, Psychology, Tempe, USA
3University of Arizona College of Medicine, Child Health, Phoenix,
USA
4Phoenix Children’s Hospital, Barrow Neurological Institute, Phoe-
nix, USA
Increasing prevalence of traumatic brain injury (TBI) and comorbid
anxiety disorders such as post-traumatic stress disorder (PTSD)
warrants attention for better understanding of underlying patho-
mechanisms. The amygdala is involved in processing emotional and
stressful stimuli and is implicated in anxiety disorders, like PTSD.
The basolateral amygdala (BLA) receives rich inputs from sensory
and limbic structures and modulates stress, fear, and emotional
learning and memory. Structural plasticity within amygdala circuits
may underlie emotional sequelae of TBI. The purpose of this study
was to quantify temporal changes in dendritic complexity of excit-
atory neurons in the BLA after TBI. Adult male rats were subjected
to a diffuse brain injury by midline fluid percussion or a sham injury.
At post-injury days (PID) 1, 7 and 28, brain tissue from sham and
brain-injured rats was processed for Golgi or silver stain, and ana-
lyzed to quantify BLA dendritic complexity in pyramidal and stellate
neurons and regional neuropathology, respectively. Compared to
sham, brain-injured rats at all PID investigated showed enhanced
dendritic complexity proximal to the soma, and at later time points at
distal portions in both BLA cell types as revealed by Sholl analysis.
However, the BLA was spared from neuropathology demonstrated
by limited argyrophilic accumulation at all time points measured, in
contrast to other regions. These data suggest an immediate and
chronic enhancement of dendritic complexity within the BLA after a
single TBI, without neuropathology. Increased dendritic complexity
would alter information processing into and through the amygdala,
which may contribute to affective symptoms after TBI, and possibly
the development of PTSD.
Supported by: NIH R03 NS-077098; Phoenix Children’s Hospital
Mission Support Funds; School of Life Sciences Undergraduate Re-
search Program at ASU
Keywords: amygdala, structural plasticity, emotion, post traumatic
stress disorder
A8-10
INDUCED MOTOR NEURON DIFFERENTIATION FROM
ENDOGENOUS NEURAL STEM CELLS IN MICE AFTER
SPINAL CORD INJURY
Yan Hao1,2, Junling Gao1, Le Wang1,3, Tiffany Dunn1, Javier Allende-
Labastida1, Jigong Wang1, Gregory Hargett1, Susan Carlton1, Jinmo
Chung1, Shaoyu Liu3, Shiqing Feng2, Ping Wu1
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