Uniformed
Services
University
9th Annual
Amygdala, Stressand PTSD Conference:
Bench to Bedside
Center for the Study of Traumatic Stress

9th Annual Amygdala, Stress and
PTSD Conference: Bench to Bedside
April 22, 2014
Sanford Auditorium & Lobby, Building B
Uniformed Services University
Bethesda, MD

www.Amygdalaptsdconference.org
Sponsored by:
The Center for the Study of Traumatic Stress (USU), Department of Psychiatry (USU),
Neuroscience Program (USU), Department of Family Medicine (USU), andDepartment of Psychiatry (WRNMMC)

1

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside2

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Uniformed Services University
Center for the Study of Traumatic Stress

9th Annual Amygdala, Stress and
PTSD Conference: Bench to Bedside
April 22, 2014
Sanford Auditorium & Lobby, Building B
Uniformed Services University
Bethesda, MD

www.Amygdalaptsdconference.org
Sponsored by:
The Center for the Study of Traumatic Stress (USU), Department of Psychiatry (USU),
Neuroscience Program (USU), Department of Family Medicine (USU), andDepartment of Psychiatry (WRNMMC)

3

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Background and Conference Committee
Background
The Amygdala Conference series is sponsored by the Center for the Study of TraumaticStress under the direction of Robert J. Ursano, MD, the USU Graduate Neuroscience
Program under the direction of Sharon L. Juliano, PhD, and also by the Department of
Family Medicine under the direction of Mark Stephens, MD.

Conference Committee
Robert J. Ursano, MD
Professor and Chair
Department of Psychiatry
Director
Center for the Study of Traumatic Stress
Uniformed Services University

Jeffrey L. Goodie, PhD, ABPP
CDR, USPHSAssociate Professor
Department of Family Medicine
Uniformed Services University
Rondricueas J. Barlow, TSgt, USAFNCOIC, Department of Psychiatry
Center for the Study of Traumatic Stress
Air Force Unit Fitness Program Manager
Unit Prevention Leader
Uniformed Services University

Gary H. Wynn, MD, 2014 Chairman
LTC, MC, USA
Assistant Chair, Research and Assistant Professor
Department of Psychiatry
Scientist
Center for the Study of Traumatic Stress
Uniformed Services University

Gwendolyn Morris
Program Support Specialist
Department of Psychiatry
Uniformed Services University

Mary Lee Dichtel, RN
Senior Medical Editor
Program Coordinator
Educational Support Management Services, LLC

Suzanne B. Bausch, PhD
Associate Professor and Vice Chairman
Department of Pharmacology
Uniformed Services University

K. Nikki Benevides, MA
Assistant to the Director and Scientific Program
Coordinator
Center for the Study of Traumatic Stress
Department of Psychiatry
Uniformed Services University
Kwang Choi, PhD
Assistant Professor
Department of Psychiatry and Program in
Neuroscience
Center for the Study of Traumatic Stress
Uniformed Services University

We extend special thanks to:
Gina Carlton, CMP, CGMP
Meetings Manager
Office of Education and Meetings
Henry M. Jackson Foundation for the 		
Advancement of Military Medicine

49th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Table of Contents
Small Table Discussion Groups.................................................................................... 2
Agenda............................................................................................................................. 3
Conference Speakers...................................................................................................... 4Moderators...................................................................................................................... 7
Conference Leadership.................................................................................................. 9
Conference Posters....................................................................................................... 11
Continuing Education Credit..................................................................................... 25

1

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Small Table Discussion Groups
Small Dining Room 0800–0900
USU Cafeteria
Please join our small group discussions from 0800–0900 in the Small Dining
Room of the USU cafeteria, Building B. Each of the conference speakers will
be available for more personalized and direct interaction with conference
attendees. Separate registration for the discussion sessions is not necessary.
Everyone registered for the conference is welcome and encouraged to attend.

Speakers
Table 1: Israel Liberzon, MD
Contextual Processing in PTSD in Humans and in the
Animal Model

Table 4: Joel Gelernter, MD
PTSD and Genetics: GxE and GWAS PTSD Studies
Table 5: Joel E. Kleinman, MD, PhD
Genetic Neuropathology in Human Brain Development and Schizophrenia: A Road Map for PTSD

Table 2: Alexander D. Crawford, PhD
High-throughput Behavioral Assays in Zebrafish: A
New Tool in the Search for Effective PTSD Therapies?
Table 3: Joshua G. Corbin, PhD
Genetic and Cellular Development of the Amygdala29th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

AGENDA
0800–0900:

Registration, Small Group Discussions and Poster Review

0900–0905:

Conference Announcements, Gary H. Wynn, MD

0905–0915:

Welcome and Introduction, Robert J. Ursano, MD

0915–1000:

Israel Liberzon, MD Contextual Processing in PTSD in Humans and in the 			Animal Model

1000–1045:

Alexander D. Crawford, PhD High–throughput Behavioral Assays in Zebrafish: 		A New Tool in the Search for Effective PTSD Therapies?

1045–1115:

Coffee Break and Poster Review in Lobby

1115–1145:

Discussion Panel 1 Moderator, LTC Dennis McGurk, PhD

1145–1245:

Lunch

1245–1330:

Joshua G. Corbin, PhD Genetic and Cellular Development of the Amygdala

1330–1415:

Joel Gelernter, MD PTSD and Genetics: GxE and GWAS PTSD Studies

1415–1445:

Coffee Break and Poster Review in Lobby

1445–1530:

Joel E. Kleinman, MD, PhD Genetic Neuropathology in Human Brain Development 		
and Schizophrenia: A Road Map for PTSD

1530–1600:

Discussion Panel 2 Moderator, LTC Christopher G. Ivany, MD

1600–1615:

Closing Remarks and Presentation of Travel Award, Robert J. Ursano, MD

39th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Conference Speakers
Joshua G. Corbin, PhD

Alexander D. Crawford, PhD

Dr. Corbin is a Principal
Investigator at the Center for
Neuroscience Research at Children’s National Medical Centerwith academic appointment as
Associate Professor of Pediatrics, Pharmacology and Physiology at George Washington
University’s School of Medicine
and Health Sciences. He holds a BA from Rutgers
University and PhD in neuroscience from the University of North Carolina, Chapel Hill. He completed a postdoctoral program at Mt. Sinai School of
Medicine in neuroscience and another postdoctoral
program at New York University School of Medicine
in developmental neuroscience. With more than
22 years of experience in the field of research, Dr.
Corbin’s lab is focused on the genetic and cellularbasis governing normal and abnormal developmentof the mammalian amygdala using the mouse as amodel. He also currently serves as a consultant for
public and private organizations focused on understanding and treating a variety of neurodevelopmental disorders. He has served as a panel reviewer for
the NIH, NSF, Autism Speaks and Department of
Defense. Dr. Corbin also had the pleasure of presenting his work to Prince Philip, Duke of Edinburgh, during the Royal visit to the US in 2007.

Dr. Crawford is Principal
Investigator of the Chemical Biology Group at
the Luxembourg Centre
for Systems Biomedicine(Esch-sur-Alzette, Luxembourg), and Senior Scientist at the Laboratory for
Molecular Biodiscovery
at the University of Leuven (Leuven, Belgium). He
is also Project Manager of PharmaSea, a European
Union-funded research consortium focusing on
drug discovery from marine microorganisms, and is
the founding CEO of Theracule, a spin-off company
focusing on personalized drug discovery and orphan
drug development for genetic CNS disorders. Dr.
Crawford was previously the founding CEO of two
drug discovery companies in Germany that raised
more than $100 million in private equity, and held
research positions at the Flanders Institute for
Biotechnology (Leuven, Belgium) and the Whitehead Institute for Biomedical Research (Cambridge,
Massachusetts). He earned a PhD in pharmaceuticalsciences at the University of Leuven, an MPhil inneuroscience at the Max Planck Institute for Developmental Biology (Tübingen, Germany), and an SB
in biology at the Massachusetts Institute of Technology.

Email: JCorbin@childrensnational.org

Website: crawfordlab.org

Websiteswww.childrensnational.org/research/faculty/bios/
cnr/corbin_j.aspx
www.gwumc.edu/smhs/facultydirectory/
profile.cfm?empName=Joshua%20Corbin&FacID=2062669303&show=1
4

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Joel Gelernter, MD

Joel E. Kleinman, MD, PhD

Dr. Gelernter is Foundations
Fund Professor of Psychiatry
and Professor of Genetics and
Neurobiology and Director,
Division of Human Genetics(Psychiatry), at Yale University
School of Medicine. He studied
music and biology as an undergraduate at Yale University
and completed his MD at SUNY-Downstate. Dr.
Gelernter began his psychiatry residency at Western Psychiatric Institute and Clinic (Pittsburgh)and completed his residency and fellowship at the
NIMH. He returned to Yale in 1988 to join the psychiatry faculty.
The research focus of his laboratory is geneticsof psychiatric illness. This includes a range of behavioral phenotypes including posttraumatic stressdisorder (PTSD), cocaine, opioid, nicotine, and alcohol dependence, panic and other anxiety disorders,schizophrenia, and affective disorders. In addition,
the lab studies a range of intermediate phenotypes,
such as neuroimaging measures; and basic issues in
population and complex trait genetics.
The overall approach involves study of genetic
polymorphism and sequence variation, on a molecular level, and from the perspective of population
genetics. Current projects include NIDA, NIAAA,
and VA-funded multicenter studies with the goal ofidentifying genes predisposing to cocaine, opioid,
nicotine, and alcohol dependence, and PTSD (using
genomewide association analysis, whole exome andwhole genome sequencing, and other approaches);
and an international drug dependence genetics
training project in collaboration with Chulalongkorn Faculty of Medicine (Bangkok, Thailand).
In the past year, Dr Gelernter’s laboratory has
published the first genomewide association studies(GWAS) for cocaine and opioid dependence, thesecond (and largest to date) for PTSD, as well as thelargest such study for alcohol dependence. All ofthese studies have resulted in the identification ofnovel risk loci.

Dr. Joel Kleinman is Associate Director, Clinical
Sciences, Lieber Institutefor Brain Development(LIBD), Johns Hopkins
University, Baltimore, MD.
Dr. Kleinman received threedegrees from the Universityof Chicago (BS, 1966, MD,
1973 and PhD, 1974). He completed an internshipat San Francisco General Hospital and residencies
in psychiatry at Harvard University and neurology
at George Washington University, respectively. He
subsequently was a tenured Section Chief in the
NIMH. Dr. Kleinman has spent the last 36 years in
the NIH amassing what is widely regarded as one of
the best collections of postmortem human brains forthe study of the molecular biology of brain development and related disorders, especially schizophrenia.
He has been both a pioneer and leader in this areaof research with over 200 peer-reviewed papers on
postmortem human brain. Recently, his research has
focused on allelic variation, alternative transcripts
and epigenetic modifications in both human brain
development and schizophrenia. His laboratory has
published a dozen papers that focus on prenatal
brain development and its importance in risk forschizophrenia. Dr. Kleinman and his group at LIBD
have also established one of the first, if not largest
collections of postmortem brains of patients withpost traumatic stress disorder.
Website: www.libd.org

Website: psychiatry.yale.edu/people/joel_gelernter.
profile5

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Israel Liberzon, MD

group. Dr. Liberzon’s primary research interest
centers on emotions, stress and stress related disorders like PTSD, and regulation and dysregulation ofstress response systems. His work integrates cognitive, functional neuroimaging, neuroendocrinological and genetic approaches to study stress, emotions,
cognitive-emotion interactions and the effects ofemotions on decision making. In the last fifteen
years, under Dr. Liberzon’s leadership, the TSARG
had be continuously funded with multiple NIMH
RO1 grants, VA Career development and NIH K
awards, VA merit awards, Army and DOD grants,
and more. Currently there are over ten active federally funded grants of various kinds awarded to Trauma Stress and Anxiety Research Group members.
Dr. Liberzon has mentored twelve doctoralcandidates, more than twenty post-doctoral research
fellows, and fourteen junior faculty members. He
has published over 150 articles, and has authoredand edited numerous book chapters and reviews.
Until recently Dr. Liberzon served as a Chief ofMental Health Service at the Ann Arbor VA Health
System. He is a Fellow of American College of
Neuropsychopharmacology. Dr. Liberzon is past
President of Psychiatric Research Society. He is an
editorial Board member for Biological Psychiatry,
Neuropsychopharmacology and other journals, andis also a member of an NIMH study section.

Dr. Liberzon is Professor of
Psychiatry, Psychology and
Neuroscience at the University of Michigan. He is also an
Associate Chair for Academic
Development and Directorof the Psychiatric Residency
Research Track at the Department of Psychiatry, Universityof Michigan. After graduating from Sacklers Medical
School, Tel Aviv University, Dr. Liberzon completed
his post-doctoral training in physiology at Rappaport Institute, Israeli Institute of Technology in
Haifa. He then completed the Psychiatry Residency
Program at the University of Michigan. Since 1992,
Dr. Liberzon has been on the faculty of the University of Michigan’s Department of Psychiatry, Department of Psychology and Neuroscience programs.
In 1992, Dr. Liberzon established the PTSD
program at the University of Michigan and Ann
Arbor VAMC, a program that has since grown andremained on the forefront of biological researchof PTSD worldwide. Dr. Liberzon co-founded
the Trauma, Stress, and Anxiety Research Group(TSARG) at the University of Michigan, which
includes the Psychiatric Affective Neuroimaging
Laboratory, a basic science (wet bench) laboratory,a MiRRR genetic repository and a clinical research

Website: sitemaker.umich.edu/panlab/home69th Annual Amygdala, Stress and PTSD Conference: Bench to BedsideModerators
Lieutenant Colonel Christopher G. Ivany, MD

Lieutenant Colonel Dennis McGurk, PhD

Dr. Christopher Ivany is
Chief of the Behavioral
Health Division at the
Office of the Army Surgeon
General and Army Directorof Psychological Health.
Dr. Ivany was born inMadison, WI. He attended
Providence College where
he majored in Biology and earned his Army commission through ROTC in 1997. Dr. Ivany attended
medical school at the University of Texas, Health
Science Center in San Antonio, TX and graduatedin 2001. He completed his internship and residency
in Psychiatry at Walter Reed Army Medical Center,
where he served as Chief Resident from 2004–2005.
In 2007, he completed a fellowship in Child and Adolescent Psychiatry at Tripler Army Medical Centerin Honolulu, HI. Dr. Ivany was assigned to Ft. Hood,
TX where he served as the 4th Infantry Division
Psychiatrist. He deployed with 4ID to Baghdad for
OIF 07-09. In 2009, Dr. Ivany and his family moved
to Ft. Carson, CO. From 2010 to 2012, Dr. Ivany
served as the Chief of the Department of Behavioral
Health at Evans Army Community Hospital. Dr.
Ivany has several publications in national peer-reviewed journals. He also has several professionalrecognitions and military awards, including theBronze Star.

Dr. McGurk is Deputy
Director of the Research
Area Directorate (RAD3),
Fort Detrick, Maryland.
The RAD3 is responsible
for managing research todevelop effective medical
countermeasures against
combat and operational
stressors to maximize warrior health and performance. Dr. McGurk was born in New Jersey. He
earned a bachelors degree in Psychology from the
University of Delaware. He began his military careerin 1989 as an Infantryman in the Army Reserve. Dr.
McGurk earned a Masters Degree in Clinical Psychology and completed ROTC at Loyola College in
Maryland. He was commissioned in 1994. Dr. McGurk’s early assignments include treatment platoon
leader at Schofield Barracks, Hawaii and Company
Commander at Walter Reed. He completed his PhD
in Experimental Psychology from Texas Tech University in 2002. Dr. McGurk commanded the U.S.
Army Medical Research Unit-Europe and was theChief of the Research Transition Office (RTO), Walter Reed Army Institute of Research. While deployed
he was the Senior Science Officer on Mental Health
Advisory Team IIb (MHAT IIb) in Afghanistan,
MHAT IV in Iraq, MHAT V in Afghanistan, andTeam Lead on the 2012 J-MHAT 8 in Afghanistan.
Dr. McGurk has published in peer-reviewed
journals and presented at scientific and militaryconferences. He has briefed many senior militaryleaders including the Under Secretary of Defense
for Personnel and Readiness and the Secretaries of
the Army and Navy. His military awards include theMeritorious Service Medal, the Army CommendaContinued
79th Annual Amygdala, Stress and PTSD Conference: Bench to BedsideDennis McGurk, PhD, Continued
the Afghanistan Campaign Medal, the Iraq Campaign Medal, the Global War on Terrorism Medal,
the Overseas Ribbon, the Air Assault Badge, and theAirborne Badge.

tion Medal, the Joint Achievement Medal, the Army
Achievement Medal, the Humanitarian Service
Medal, the Armed Forces Expeditionary Medal, theNATO Kosovo Medal, the Kosovo Campaign Medal,

89th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Conference Leadership
Lieutenant Colonel Gary H. Wynn, MD

Robert J. Ursano, MD

Dr. Wynn is Assistant Chair ofResearch and Assistant Professor, Department of Psychiatry,
Uniformed Services University and Scientist, Centerfor the Study of TraumaticStress. After graduating from
West Point in 1996, Dr. Wynn
received his medical degree in2000 from the Uniformed Services University (USU)
in Bethesda, MD. Dr. Wynn completed a combined
residency in Psychiatry and Internal Medicine at
Walter Reed Army Medical Center. After completing his residency, he spent a year as the Division
Psychiatrist for the 2nd Infantry Division at Camp
Casey, Korea. Dr. Wynn spent the next three years
as the Assistant Chief of Inpatient Psychiatry at
Walter Reed Army Medical Center where he worked
with service members returning from the conflicts
in Iraq and Afghanistan. From 2009 through 2013,
Dr. Wynn worked as a research psychiatrist in the
Military Psychiatry Branch of the Center for Military Psychiatry and Neuroscience at the Walter Reed
Army Institute of Research in Silver Spring, MD. In
July, 2013, Dr. Wynn joined the USU Department of
Psychiatry. He has published textbooks on the topics
of drug interaction principles for medical practiceand the clinical management of post traumatic stressdisorder (PTSD) as well as numerous book chaptersand journal articles. His presentations at numerous
national and local conferences have covered topics
ranging from drug interactions to PTSD and mild
traumatic brain injury.

Dr. Ursano is Professor of
Psychiatry and Neuroscience
and Chairman of the Department of Psychiatry at the
Uniformed Services University of the Health Sciences,
Bethesda, Maryland. He is
founding Director of Centerfor the Study of TraumaticStress. In addition, Dr. Ursano is Editor of Psychiatry, the distinguished journal of interpersonal andbiological processes, founded by Harry Stack Sullivan. Dr Ursano completed twenty years of service in
USAF medical corps and retired as Colonel in 1991.
He was educated at the University of Notre Dameand Yale University School of Medicine and did his
psychiatric training at Wilford Hall USAF Medical
Center and Yale University.
Dr. Ursano served as the Department of Defense
representative to the National Advisory Mental
Health Council of the National Institute of Mental
Health and is a past member of the Veterans Affairs
Mental Health Study Section and the National Institute of Mental Health Rapid Trauma and Disaster
Grant Review Section. He is a Distinguished Life
Fellow in the American Psychiatric Association. He
is a Fellow of the American College of Psychiatrists.
Dr. Ursano was the first Chairman of the American
Psychiatric Association’s Committee on PsychiatricDimensions of Disaster. This work greatly aided theintegration of psychiatry and public health in timesof disaster and terrorism. Dr. Ursano was an invited participant to the White House Mental HealthConference in 1999. He has received the Department of Defense Humanitarian Service Award andthe highest award of the International TraumaticContinued
99th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Robert J. Ursano, MD, Continued
Stress Society, The Lifetime Achievement Award,
for “outstanding and fundamental contributions tounderstanding traumatic stress.” He is the recipientof the William C. Porter Award from the Association of Military Surgeons of the United States, and afrequent advisor on issues surrounding psychological response to trauma to the highest levels of the US
Government and specifically to the Department of
Defense leadership.
Dr. Ursano has served as a member of the National Academies of Science, Institute of Medicine,Committee on Psychological Responses to Terror-ism, Committee on PTSD and Compensation and
the Committee on Nuclear Preparedness; and the
National Institute of Mental Health Task Force on
Mental Health Surveillance After Terrorist Attack. In
addition he is a member of scientific advisory boards
to the Secretary of Health and Human Services andthe Centers for Disease Control. In 2012, Dr. Ursano
was awarded the William C. Menninger Memorial
Award for distinguished contributions to the Scienceof Mental Health by the American College of Physicians. Dr. Ursano has more than 300 publications.
He is co-author or editor of eight books.

109th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Conference Posters
Presented in Lobby
Travel Award Winner
Impaired Extinction Retention in Patients Who Developed PTSD Following aSingle Traumatic Event................................................................................................... 12

Posters

Posttraumatic Stress MicroRNA Signatures in Serum and Amygdala of Rats:
Potential Role in Fear Mechanism(s) and Biomarker Development........................ 13
Individual Differences in Morphine Self-Administration Predict Body Weight
Change, Acoustic Startle Reflex and Drug Seeking Behavior During
Spontaneous Withdrawal from Morphine................................................................... 14
Transcriptome Analysis of Discrete Microdissected Amygdala and otherRegions of Fresh and Frozen, Intact non-Human Primate Brain............................. 15
Cytokine and Chemokine Profiling of Plasma and CSF Identifies the
MCP-4/MCP-1 Ratio as a Novel Diurnal Candidate Plasma Biomarker
for Chronic Post-Traumatic Stress Disorder............................................................... 16
Neuronal Morphology and Cell Signaling Transcripts are Differential Markers
in Hippocampal Transcriptomes of Fear-Resilient Mice During Fear
Conditioning.................................................................................................................... 17
Spontaneous Withdrawal from Chronic Morphine Self-Administration Reducesin vivo Brain Glucose Metabolism (18FDG-PET) and Facilitates Fear
Extinction in Rats............................................................................................................ 18
Mitochondrial Gene Expression Profiles and Metabolic Pathways in the
Amygdala Associated with Exaggerated Fear in an Animal Model of PTSD......... 19
Sex Differences in the Single Prolonged Stress (SPS) Model of PosttraumaticStress Disorder (PTSD).................................................................................................. 20
Synaptic Potentiation in Medial Amygdala Related to Anger........................................... 21
Multimodal in vivo Imaging Reveals Structural and Functional Changes in the
Amygdala of a Controlled Cortical Impact Small Animal Model of Traumatic
Brain Injury...................................................................................................................... 22
Characterization of Psychological and Biological Factors 23 in an Animal
Model of Warrior Stress.................................................................................................. 23
Roles of p11 in Memory Retrieval: A Behavior Test of p11 Knock-Out Mice................ 24

11

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Travel Award Winner
Impaired Extinction Retention in Patients Who Developed
PTSD Following a Single Traumatic Event
Authors

Method: Thirty-eight participants diagnosed with
PTSD were classified into one of two groups—Single
Trauma (n=19) or Multiple Trauma (n=19)—basedon self-reported trauma exposure history prior to
PTSD onset. A 2-day Pavlovian threat-conditioning
procedure with skin conductance response (SCR)
was used to examine differences in threat conditioning, extinction learning, and extinction retention
between the two groups.

Heather L. Rusch, MS , Erel Shvil, PhD , Miriam
Campeas, BS1, Emily D. Joyner, BS1, Jessica M. Gill,
PhD2, Mohammed R. Milad, PhD5, Gregory M.
Sullivan, PhD1,4, Yuval Neria, PhD1,4
1,2,3

1,4

Affiliations

1. New York State Psychiatric Institute, New York,NY
2. National Institute of Nursing Research, National
Institutes of Health, Bethesda, MD
3. Henry M Jackson Foundation for The Advancement of Military Medicine, Bethesda, MD
4. Department of Psychiatry, Columbia University
Medical Center, New York, NY
5. Department of Psychiatry, Harvard Medical
School & Massachusetts General Hospital,
Boston, MA

Results: No significant demographic (i.e., gender,
education, and age), clinical (i.e., depression and
PTSD symptom severity), or shock level differenceswere found between the two groups, with the exception of ethnicity. On Day 1, both groups acquired
the CS-US contingency and achieved comparable
extinction learning. During the early extinction
recall phase on Day 2, the Multiple Trauma groupexhibited lower SCR (i.e., less startle) to the previously extinguished stimulus (CS+E) comparedwith the non-extinguished stimulus (CS+NE),
thus demonstrating intact retention of extinction
learning. Meanwhile, the Single Trauma groupevinced comparable responses to both the CS+E andCS+NE, suggesting impaired extinction retention.

Abstract
Background: While the risk for posttraumatic stressdisorder (PTSD) increases with multiple traumatic exposures, a swubstantial proportion of trauma
exposed individuals demonstrate a heightened
vulnerability to trauma by developing PTSD after asingle, time limited, traumatic incident. To advanceresearch on putative biomarkers of this increased
vulnerability, the current study investigated whether PTSD patients reporting a single traumatic
event exhibited greater extinction retention deficits
compared to PTSD patients who endured multiple
traumatic events before developing PTSD.

Conclusion: The study results suggest for the firsttime that while PTSD patients with multiple trauma
exposures exhibit intact extinction retention, those
who developed PTSD following a single traumatic
incident revealed impaired extinction retention. The
findings underscore the complex nature of PTSD,
and warrant further examination of whether patientswith a lower threshold for developing PTSD have adecreased capacity to process traumatic experiences.
12

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Posttraumatic Stress MicroRNA Signatures in Serum andAmygdala of Rats: Potential Role in Fear Mechanism(s)and Biomarker Development
Authors

0 and day 14 of serum and amygdala was analyzed
using Taqman low-density real time PCR arrays. A
panel of nine stress-responsive miRNAs viz., miR142-5p, miR-19b, miR-1928, miR-223-3p, miR-322*,
miR-324, miR-421-3p and miR463* and miR-674*
were identified as potential biomarker candidates for
PTSD. Most miRNAs were found to be downregulated at day 0 immediatley after the cessation of stressin amygdala. An increase in total miRNAs was observed at day 14 amygdala which suggest a substantial alteration of the posttranscriptional machineryand indicate that the newly formed fear memories
are being consolidated into stable long-term memories in the amygdala during PTSD development.
Further validations by bioinformatics and system
biology approaches identified five miRNAs, miR142-5p, miR-19b, miR-1928, miR-223 and miR-4213p, which may play a role in the regulation of genes
associated with delayed and exaggerated fear. To thebest of our knowledge, this is the first report demonstrating the plausibility of using circulating miRNAs
as biomarkers of PTSD.
The views presented here are of the authors andshould not be construed as that of DMRDP, USUHSor BITS Pilani. These studies were supported byfunding form DMDRP (PI: Radha K.Maheshwari)

Nagaraja S. Balakathiresan1, Raghavendar Chandran1,2, Manish Bhomia1,2, Anuj Sharma1, Min Jia3,
He Li3 and Radha K. Maheshwari1

Affiliations

1. Department of Pathology, Uniformed Services
University, Bethesda, MD
2. Biological Sciences Group, Birla Institute of Technology and Science, Pilani, Rajasthan 333031,
India
3. Department of Psychiatry, Uniformed Services
University, Bethesda, MD

Abstract

The molecular mechanism(s) underlying fear
response due to acute traumatic stress and anxiety
disorder is not clearly understood. MicroRNAs are
post-transcriptional regulators of gene expression
including genes of the serotonergic system. The primary aim of this study was to identify the candidate
miRNA(s) as diagnostic biomarker in the serum
and their involvement in fear memory formationin the amygdala. MiRNA expression in serum andamygdala of rats was studied which were exposed totraumatic stress for three days, using a restraint and
tail shock model. Global miRNA expression at day

13

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Individual Differences in Morphine Self-Administration Predict
Body Weight Change, Acoustic Startle Reflex and Drug Seeking
Behavior During Spontaneous Withdrawal from Morphine
Authors

weight and drug intake were monitored daily. The
ASR and drug seeking were measured during the
spontaneous withdrawal from chronic MSA.
Results On average, morphine animals did not gain
weight (101%±0.69) while the saline control animals
did (115%±1.06) after 3 weeks of self-administration. However, individual differences in initial morphine intake (first 10 minutes), but not total intake(4 hours), were positively correlated with the weightchange in morphine animals (r: 0.428, p: 0.033). Although the average ASR were not significantly different between the morphine and the control animals,
the initial morphine intake was negatively correlatedwith the ASR in morphine animals (r: -0.544, p:
0.005). On the contrary, the initial morphine intake
was positively correlated with drug seeking behavior during the spontaneous withdrawal (r: 0.424, p:
0.035).

Kwang Choi1,2,3, Thien Le1,2, Mercedes Xia1,2, Min
Jia1,2, He Li1,2,3 and Robert J. Ursano1,2,3

Affiliations

1. Department of Psychiatry, Uniformed Services
University, Bethesda, MD
2. Center for the Study of Traumatic Stress, Department of Psychiatry, Uniformed Services University, Bethesda, MD
3. Program in Neuroscience, Uniformed Services
University, Bethesda, MD

Abstract

Rationale: Although chronic use of and withdrawal
from opiates can cause undesirable side effects suchas weight loss, anxiety and craving for drugs, potential individual differences contributing to theseeffects are largely unknown.

Conclusions: We found that individual differences in initial morphine intake can predict weightchange, acoustic startle (anxiety) and craving for
drug during the spontaneous withdrawal. A subgroup of animals appear to be more sensitive toreinforcing effects while more tolerant to aversive effects of morphine. Identifying individual differencesin opioid responses may provide a novel treatment
strategy for anxiety and substance use disorders.
Supported by the CSTS.

Objectives: We investigated whether individual
differences in intravenous morphine self-administration (MSA) are associated with body weightchange, acoustic startle reflex (ASR) and drug seeking behavior during spontaneous withdrawal frommorphine.
Methods: Male Sprague Dawley rats self-administered either morphine (0.5 mg/kg/infusion) or saline
for 3 weeks (4 hours/day, 5 days per week) and body14

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Transcriptome Analysis of Discrete Microdissected
Amygdala and other Regions of Fresh and Frozen,
Intact non-Human Primate Brain
Authors

non-parallel and not optimal for low abundance
transcripts. Here, we have implemented a workflow
to obtain discrete areas of either fresh or frozen
non-human primate brain by targeted sectioning
and micropunching to isolate high integrity RNA for
profiling by massive parallel sequencing. We have
utilized this strategy to prepare sequencing libraries
from orbital-frontal cortex, medial frontal cortex(Area 25), anterior cingulate cortex, insular cortex,
amygdala, hippocampus and entorhinal cortex from
non-human primate brain. In each of these anatomical regions, we have determined the complete
transcriptome at high sequencing depth (up to 60
million reads). Comparative transcript expression
analysis of multiple subjects identified previously
known and candidate novel transcript features withincreased or specific expression in distinct brain
regions. These transcripts are enriched in known
functions for energy metabolism, neurotransmitter
signaling, and neuronal morphology. This developed microdissection technique provides a workflow to permit experimental access to central brain
regions that may be analyzed in context of acquiredor endogenous injury or disease. This simple methodology may be utilized to provide a transcriptomic
data complement to behavioral or connectomics
studies that store disease-specific brains in biologicalrepositories.

Clifton L. Dalgard, PhD , Harvey B. Pollard, MD ,Vijay Singh, PhD2, Kadharbatcha S. Saleem, PhD3,
Robert J. Ursano, MD4, David M. Jacobowitz, PhD1
1

1

Affiliations

1. Department of Anatomy, Physiology and Genetics, and Center for Medical Proteomics, Uniformed Services University School of Medicine,
4301 Jones Bridge Rd, Bethesda, MD 20814
2. Department of Radiation Biology, Armed Forces
Radiobiological Institute (AFRRI), Uniformed
Services University, 4301 Jones Bridge Rd,
Bethesda, MD 20814
3. National Institute of Neurological Diseases andStroke, National Institutes of Health, 9600 Rockville Pike, Bethesda, MD 20892
4. Department of Psychiatry and Center for the
Study of Traumatic Stress, Uniformed Services
University School of Medicine, Uniformed Services University, 4301 Jones Bridge Rd, Bethesda,
MD 20814

Abstract

Genomic and proteomic profiling of subcorticalregions from intact human and non-human primate
brain present specific technical problems that limit
accuracy and sensitivity. In situ hybridization, while
maintaining spatial precision, is low throughput,

15

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Cytokine and Chemokine Profiling of Plasma and CSF Identifies
the MCP-4/MCP-1 Ratio as a Novel Diurnal Candidate Plasma
Biomarker for Chronic Post-Traumatic Stress Disorder
Authors

exposure to traumatic events. PTSD may be acute or
chronic, and can have a waxing and waning courseof symptoms. It has been hypothesized that proinflammatory cytokines and chemokines in the CSF or
plasma might be biomarkers, surrogates, or drivers
for the psychophysiological mechanisms relating ahistory of trauma exposure to changes in behavior
and mental health disorders and medical morbidity.

Clifton Dalgard , Ofer Eidelman , Catherine
Jozwik1,2, Yvonne K. Eudy1,2, Meera Srivastava1,2,
Roopa Biswas1,2, Stephen W. Rothwell1,2, Gregory P.
Mueller1,2, Peixiong Yuan3, Wayne Drevets3,4, Husseini K. Manji3,4, Meena Vythilingam3,5, Dennis S.
Charney3,6 , Robert J. Ursano7,8, David M. Jacobowitz1,2, Harvey B. Pollard1,2, and Omer Bonne3,9
1,2

1,2

Hypothesis: Here, we further test the cytokine/
chemokine hypothesis for PTSD by examining levelsof 17 classical cytokines and chemokines in CSF,
sampled at 9 AM, and in plasma sampled hourly
over a 24 hour period.

Affiliations

1. Department of Anatomy, Physiology and Genetics, Uniformed Services University School of
Medicine, Bethesda, MD
2. Center for Medical Proteomics, Uniformed Services University School of Medicine, Bethesda,
MD
3. Mood and Anxiety Disorders Branch, National
Institute for Mental Health, Bethesda, MD
4. Janssen Research and Development, Titusville,
NJ
5. Office of Deputy Assistant Secretary of Defense ,Department of Defense, Washington, DC 20307
6. Mount Sinai School of Medicine, New York, NY
7. Department of Psychiatry, Uniformed Services
University School of Medicine, Bethesda, MD
8. Center for the Study of Traumatic Stress, Uniformed Services University School of Medicine,
Bethesda MD
9. Department of Psychiatry, Hadassah Medical
Center, Jerusalem, Israel

Methods: The PTSD and healthy control patientsare all from the chronic PTSD (N = 12) and Healthy
Control (N=11) cohort, initially described by Bonneet al (2011). We quantitatively measured cytokinesand chemokines using a MesoScale multiplexed
electrochemiluminescent ELISA platform.
Results: We find that in plasma, collected hourly
over a 24 hour period, the bivariate MCP4/MCP1
ratio significantly discriminates between PTSD and
Healthy Control patients at all time points. At the 9
AM time point, the MCP-4/MCP-1 ratio in PTSD
plasma is elevated 66% (p = 0.004; AUC = 0.84). In
CSF, collected at 9 AM from the same patients, wefind that the MCP-4/MCP-1 ratio is not informative.
Conclusion: The ratio of MCP-4/MCP-1 in plasma
may be a biomarker for PTSD in civilian PTSD patients that is invariant over a 24 hour period.

Abstract

Background: Post-traumatic stress disorder (PTSD)
is a psychiatric disorder, which occurs following

16

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Neuronal Morphology and Cell Signaling Transcripts are
Differential Markers in Hippocampal Transcriptomes of FearResilient Mice During Fear Conditioning
Authors

and low levels of fear. These fear susceptible and fear
resilient mice were previously utilized to identify
candidate genes that contribute to baseline susceptibility or resilience to fear establishment. Functional
imaging in these mice demonstrated differential
activity in the hippocampus of the fear susceptible
mice, which amygdala activity was non-significantly
different. To investigate the mechanisms underlying this difference in activity we performed complete transcriptome profiling using next generation
sequencing of hippocampal tissue from these miceand performed differential expression analysis to
identify candidate transcripts which are associatedwith functional activity differences observed. An
enrichment of transcripts associated with neuronalmorphology, GSK-3b associated cellular signaling
and axonal transport. Comparative analysis of transcriptomes as a function of fear conditioning exposure revealed a distinct subset of transcript featuresenriched for neuronal function. We anticipate thatfunctional analysis of these candidate transcripts
for fear phenotypes will elucidate novel strategies
to mitigate deleterious mechanisms contributing todeveloping PTSD.

Steven C. Dash, BA , David M. Jacobowitz, PhD ,Robert J. Ursano, MD2, Clifton L. Dalgard, PhD1
1

1

Affiliations

1. Department of Anatomy, Physiology and Genetics, and Center for Medical Proteomics, Uniformed Services University School of Medicine,
4301 Jones Bridge Rd, Bethesda, MD 20814
2. Department of Psychiatry, and Center for the
Study of Traumatic Stress, Uniformed Services
University School of Medicine, 4301 Jones Bridge
Rd, Bethesda, MD 20814

Abstract

Post traumatic stress disorder (PTSD) affects
approximately 8.6% of veterans returning fromconflicts in Iraq and Afghanistan. Intrusive fearful
thoughts and memories are one of the hallmarks of
PTSD. Accordingly, animal models of fear memory
are utilized to investigate this component of PTSD
in a controlled setting. To study the mechanisms offear conditioning, which mimics certain symptomsof PTSD, an animal model was developed to create
a divergent mouse intercross line displaying high17

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Spontaneous Withdrawal from Chronic Morphine SelfAdministration Reduces in vivo Brain Glucose Metabolism(18FDG-PET) and Facilitates Fear Extinction in Rats
Authorsmorphine (0.5 mg/kg/injection) for 3 weeks (4 hr/day, 5 days/week). During the spontaneous withdrawal from the MSA, animals were tested with
Pavlovian fear conditioning and extinction. In
vivo regional glucose uptake was measured using a
combined [18F]fluoro-2-deoxy-D-glucose positronemission tomography (18FDG-PET) and computed
tomography (CT) scan before and after the MSA.

Thien Le, BS1,2, Reed G. Selwyn, PhD3, David M.
Benedek, MD1,2, Robert J. Ursano, MD1,2,4 and Kwang
Choi, PhD1,2,4

Affiliations

1. Department of Psychiatry, Uniformed Services
University, Bethesda, MD
2. Center for the Study of Traumatic Stress, Bethesda, MD
3. Department of Radiology, Uniformed Services
University, Bethesda, MD
4. Program in Neuroscience, Uniformed Services
University, Bethesda, MD

Results: Morphine animals did not show differencesin fear learning but showed facilitated fear extinction
when compared to the control animals. During thewithdrawal, in vivo glucose uptake was decreased in
the brainstem as compared to the pre-MSA baseline.
A morphine challenge (0.5 mg/kg) induced a robust
behavioral sensitization and increased in vivo glucose uptake in the nucleus accumbens, the amygdala
and the brainstem of morphine-dependent animals.

Abstract

Background: Chronic use of opiates may lead to abnormal brain energy metabolism which contributes
to increased anxiety and stress responses. However,in vivo regional glucose metabolism and fear-related behavior following chronic use of morphine arelargely unknown. Previous studies reported thatwithdrawal from repeated experimenter-administered morphine was associated with impaired fear
extinction in rats.

Discussion: Spontaneous withdrawal from chronic
opiate use may have drastic effects on brain energy
metabolism and fear/anxiety behavior. This may
partially explain the mechanisms of abnormal fear
extinction observed in morphine self-administeredanimals. By combining a clinically relevant animalmodel and a non-invasive brain imaging, we demonstrated the utility of studying important relationshipbetween in vivo brain function and psychiatric behavior. The current findings have important clinicalimplications because opioid drugs are increasingly
used as analgesics and have high abuse potential.

Method: Using an intravenous morphine self-administration (MSA) paradigm, we investigated theeffects of chronic morphine on in vivo brain glucose metabolism and fear extinction in rats. Male
Sprague-Dawley rats self-administered intravenous

18

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Mitochondrial Gene Expression Profiles and Metabolic
Pathways in the Amygdala Associated with Exaggerated
Fear in an Animal Model of PTSD
Authors

were determined using a cDNA microarray. During
the development of the exaggerated fear associatedwith PTSD, 48 genes were found to be significantly
upregulated and 37 were significantly downregulated in the amygdala complex based on stringent
criteria (p<0.01). Ingenuity Pathway Analysis (IPA)
revealed up or down regulation in the amygdalacomplex of four signaling networks – one associated with inflammatory and apoptotic pathways, onewith immune mediators and metabolism, one withtranscriptional factors, and one with chromatin
remodeling. Thus, informatics of a neuronal genearray allowed us to determine the expression profile
of mitochondrial genes in the amygdala complex ofan animal model of PTSD. The result is a further understanding of the metabolic and neuronal signalingmechanisms associated with delayed and exaggerated fear.

He Li1*, Xin Li2, Stanley E. Smerin1, Lei Zhang1, Min
Jia1, Guoqiang Xing 1, Yan A. Su3, Jillian Wen1, David
M. Benedek1 and Robert J. Ursano1

Affiliations

1. Department of Psychiatry and Center for the
Study of Traumatic Stress, Uniformed Services
University, Bethesda, MD
2. Department of Biostatistics, Bioinformatics, andBiomathematics, Georgetown University Medical
Center, 3700 O Street, N.W., Washington, D.C.
20057
3. Department of Gene and Protein Biomarkers,
GenProMarkers, 9700 Great Seneca Highway,
Rockville, MD 20850

Abstract

The metabolic mechanisms underlying thedevelopment of exaggerated fear in post-traumatic stress disorder (PTSD) are not well defined. In
the present study, alteration in the expression ofgenes associated with mitochondrial function in the
amygdala of an animal model of PTSD was determined. Amygdala tissue samples were excised from
10 nonstressed control rats and10 stressed rats, 14days post stress treatment.. Total RNA was isolated,
cDNA was synthesized, and gene expression levels

The views expressed in this article are those of theauthors and do not necessarily reflect the official
policy or position of the Uniformed Services University, Department of the Navy, Department of
Defense, nor the U.S. Government. This research
was supported by CSTS and CDMRP grant W81XWH-08-2-006 (PI: He Li).
*19

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Sex Differences in the Single Prolonged Stress (SPS)
Model of Posttraumatic Stress Disorder (PTSD)
Authors

effect in male rats, our data indicate that females
exposed to SPS do not show the enhanced stress-induced CORT suppression typical of SPS-exposedmales. This lack of an enhanced DEX suppression isakin to a “DEX non-suppression” phenotype typically associated with depression. Thus, enhanced DEX
suppression of CORT (in males) and no DEX suppression of CORT (in females) may represent twocore phenotypes of PTSD that may be segregated bygender. The acoustic startle response (ASR) measures the enhanced arousal associated with PTSD
and, as expected, we found to be exaggerated in
SPS-exposed males. However, we find that females
normally become more reactive with repeated exposure to the startle stimulus, regardless of wehther
they have been exposed to SPS. These data indicatethat female rats do not respond to SPS with the same
phenotype established in male rats, indicating thatthe traumatic stress response manifests differently
in male and female rats. Understanding the mechanisms underlying different types of PTSD response
patterns is crucial in determining effective diagnostic measures and individual treatment.

A. Pooley, S.M. Breelove, and C.L. Jordan

Affiliation

Neuroscience Program, Michigan State University,
East Lansing, MI

Abstract

Women are more than twice as likely to develop PTSD as men; however, the reasons for this sex
difference are not understood. To our knowledge,
this is the first study to systematically examine thesex-specific effects of SPS, a validated PTSD animalmodel, in adult rats. Used to detect disruption of
the hypothalamic-pituitary-adrenal (HPA) axis, thedexamethasone (DEX) suppression test indicatesthat patients with PTSD typically exhibit exaggerated suppression of cortisol in the stress response, suggesting a hypersensitivity to HPA negative feedback.
In rats, exaggerated DEX suppression of corticosterone has also been demonstrated in the SPS model,
but as with the clinical reports, this generalization
was formed with evidence from predominately malepopulations. While our data replicate the expected20

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Synaptic Potentiation in Medial Amygdala
Related to Anger
Authors

Methods: Under urethane anesthesia, the MeAof the rat is electrically stimulated (0.2–1.0mA,
0.2msec) via basomedial amygdala (BAM) afferents
or accessory olfactory bulb (AOB) afferents. The excitatory postsynaptic field potential (fEPSP) evokedby each stimulation is recorded. The stimulus isgiven at a slow enough rate (1 pulse / 10 sec) suchthat it in itself does not produce synaptic potentiation. After a baseline is collected, a brief (5 sec) burstof 200 pps is given, after which a return baseline iscollected, again at 1 pulse/10 sec.

Stanley Smerin PhD1, Michael Potegal PhD2, He Li
MD, PhD1

Affiliations

1. Uniformed Services University, Bethesda, MD
2. University of Minnesota, Minneapolis, MN

Abstract

Introduction: Anger is a devastating component of
post traumatic stress disorder (PTSD). High frequency stimulation of the medial amygdala (MeA)peaking at 200 pps accelerates aggressiveness inexperimental animals. This aggressiveness at leastappears to be a manifestation of anger and has atime course comparable to that of short term synaptic potentiation (STP).

Results: 200 pps stimulation of BAM or AOB afferents to the MeA potentiates excitatory synaptictransmission with a time course corresponding to
STP.
Conclusion: High frequency stimulation of the MeA
such as accelerates aggression in rats also evokes
STP in MeA.

Hypothesis: High frequency stimulation evokes STP
in MeA.

21

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Multimodal in vivo Imaging Reveals Structural and Functional
Changes in the Amygdala of a Controlled Cortical Impact
Small Animal Model of Traumatic Brain Injury
Authorstake. Scatter and attenuation‐corrected PET sinograms were reconstructed as a single high resolution
static frame. Multi‐echo T2‐weighted and diffusion‐weighted MRI data were acquired using a Bruker
Biospec 7T/20 scanner. Quantitative T2 and ADC
maps were generated using non-linear with constant (Levenberg-Marquardt) and linear (OLS) leastsquares estimations, respectively. A robust image
processing technique was developed to evaluate 13
brain regions for coregistered PET/CT/MR images.
Normalized FDG uptake and the average T2 andADC values were determined for the whole amygdala, ipsilateral, contralateral, and the ratio of ipsilateral to contralateral (I/C) amygdala was calculated.

Colin M. Wilson1, Shalini Jaiswal1, Fiona Brabazon3,
Sanjeev Mathur1, Alexandru Korotcov1, Asamoah
Bosomtwi1, Dinesh K. Shukla1, Elizabeth Broussard1,
Scott Jones1,2, Kimberly R. Byrnes3, Reed G. Selwyn1,2Affiliations

1. Translational Imaging Core, Center for Neuroscience and Regenerative Medicine, Bethesda, MD
2. Radiology and Radiological Sciences, Uniformed
Services University, Bethesda, MD
3. Anatomy, Physiology, and Genetics, Uniformed
Services University, Bethesda, MD

Abstract

Results: Cross‐sectional, repeat measures analysis
of each post‐injury time point relative to baseline
revealed a significant decrease (p≤0.01) in FDG
uptake at days 3 and 7, corresponding to significant
decreases in ADC and increases in T2 values. In
addition, the ratio of ipsilateral/contralateral for
FDG uptake and T2 values were highly correlated(Pearson r=‐0.937, p=0.006). Taken together, theseparameters indicate cytotoxic edema at sub-acutetime points and not swelling of extracellular space or
cellular infiltration.

Objectives: The amygdala is a region of particularinterest in the study of both traumatic injury (TBI)
and post‐traumatic stress disorder (PTSD) among
military services members. Positron emission
tomography (PET) with 18F‐fluorodeoxyglucose(FDG) and magnetic resonance (MR) imaging was
utilized to characterize rat brain injury using FDG
uptake, apparent diffusion coefficient (ADC), andT2‐relaxation time (T2).
Methods: A moderate controlled cortical impact(CCI) brain injury was conducted on male Sprague
Dawley (SD) rats with imaging performed prior to
injury (baseline) and at one other time point between 3‐6 hours and 21 days post‐injury. FDG‐PET
scans were acquired for 30 minutes on a Siemens
PET/CT scanner following 45 minutes of FDG up-

Conclusion: When combined, FDG‐PET and MR
imaging provide a remarkably sensitive method for
detecting structural and functional changes in the
amygdala after TBI.

22

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Characterization of Psychological and Biological Factors
in an Animal Model of Warrior Stress
Authors

The purpose of this project was to characterize
psychological and biological responses in a rodent
model of Warrior Stress using males and female rats.
A comprehensive and sophisticated multivariate
data analytic strategy examined complex relationships among behavioral and biological responses tophysical and psychological stress. Data were gathered from an experimental investigation of blast
overpressure induced traumatic brain injury andpsychological stress in male and female rats (N=96).
Exploratory factor analysis, multivariate analysis ofvariance, and multiple discriminant analysis were
performed to: (a) reveal underlying dimensions in
the data; (b) use those dimensions to try to identify
the mechanisms of differential effects of four levelsof stress; and (c) determine whether there were sex
differences for psychobiological variables.
Multivariate analyses revealed that males andfemales differed on dimensions that represented
neurochemical function of: (a) serotonin among
the prefrontal cortex, hippocampus, insula cortex,
and basolateral amygdala, and (b) dopamine activity among the prefrontal cortex and the amygdala.
There were no apparent differences among stressgroups on combinations of the psychobiologicalvariables. This project highlights the need for considering sex differences in psychobiological responses and for including males and female participantsin all injury and stress research.

Angela M. Yarnell, PhD1, and Neil E. Grunberg,
PhD2

Affiliations

1. Walter Reed Army Institute of Research, Silver
Spring, MD
2. Uniformed Services University, Bethesda, MD

Abstract

For over a decade, American service members
have been vigorously defending this nation and, inthe process, have been exposed to death or the threatof death, explosive blasts, debilitating injuries, andother environmental stressors (e.g., noise, heat), notto mention separation from loved ones and unpredictable deployment schedules. Because service
members are exposed to physical and psychologicalstressors, it is important to understand the effects ofstress on psychobiological processes to better prevent and/or treat resulting illness or injury. Despite
increased awareness that Warriors exposed to stressand blast may experience cognitive effects (e.g.,memory and attention problems) and other post-deployment symptoms (e.g., chronic pain) mechanisms
underlying psychological effects of stress and blast
injury have yet to be identified. Therefore, basic
research must be conducted to understand the complex response to injury and stress.

23

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Roles of p11 in Memory Retrieval: A Behavior Testof p11 Knock-Out Mice
Authors

this study, we examined p11 knock-out mice in thewater-maze spatial test to elucidate the role of p11
in memory retrieval. There were two sets of results:
control data and experimental data sets. The controls
were wild-type and p11 knockout mice, pharmacological controls (i.e., mice received saline injection)and stress controls (yoked foot shock). The experimental groups were wild-type or p11 knockout
mice, which received pharmacological treatment(corticosterone injection) and foot shock exposure.
We found that the latency to find platform was
shorter in p11 knockout mice than that in wild typemice during training day 1-3, although the latency
for both wild and knock-out was not different on
the final day of training or probe test. We also foundthat corticosterone resulted in significant decreases
in the time spent in quadrant and number of islandcrossing in both p11 knockout and wiled type control. Our data indicate that p11 knock-out enhances
memory retrieval and corticosterone induced-impairment of memory retrieval is independent of the
p11 expression.

Lei Zhang, MD1, LauraTucker, MS2, Xian-Zhang Hu,
MD, PhD1, Xiaoxia Li, BS1, He Li, MD, PhD1, 		
Stanley Smerin, PhD1, Robert J. Ursano, MD1

Affiliations

1. Center for the Study of Traumatic Stress, Department of Psychiatry, Uniformed Services
University, Bethesda, MD
2. Pre-Clinical Studies Core, Center for Neuroscience and Regenerative Medicine, Uniformed
Services University, Bethesda, MD

Abstract

Stress increases expression of p11, a member of
the S100 family of proteins and influences learningand memory. Patients with PTSD, a traumatic stressassociated disorder, have over-expressed p11 and experience fixed memory on a traumatic event so thatthe processing of non-trauma-related memories isoften impaired. However, the role of p11 in memory,
particularly in memory retrieval is still unknown. In

249th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Continuing Education Credit
PhysiciansSocial Workers

This live activity, Amygdala, Stress and PTSD Conference, on April 22, 2014 has been reviewed and isacceptable for up to 4.75 prescribed credits by theAmerican Academy of Family Physicians. Physicians
should claim only the credit commensurate with theextent of their participation in the activity.

The Department of Social Work, Walter Reed
National Military Medical Center, maintains responsibility for this program and has been granted
automatic authorization from the Maryland Boardof Social Work Examiners to offer 4.75 category I
CEU credit for this professional training activity. 2.0hours of CEU credit will be given for the morning
session and 2.75 hours of CEU credit will be given
for the afternoon session. No credit will be provided
for partial session attendance. On the day of theconference, participants must submit an evaluation
sheet for each session to receive CE credit and document their attendance for each session via sign-in
and out rosters.

Psychologists

The Department of Psychology, Walter Reed National Military Medical Center, is approved by theAmerican Psychological Association to sponsor
continuing education for psychologists. The Department of Psychology, Walter Reed National Military
Medical Center maintains responsibility for thisprogram and its contents. 4.75 hours of CE credit
will be given for full attendance at the workshop.
2.0 hours of CE credit will be given for the morning
session and 2.75 hours of CE credit will be given for
the afternoon session. No credit will be provided
for partial session attendance. On the day of theconference, participants must submit an evaluation
sheet for each session to receive CE credit and document their attendance for each session via sign-in
and out rosters.

NursesWe regret we are unable to offer CEUs for nurses in
2014. We are confident we will be able to offer CEUs
in 2015 that may meet your practice and careerneeds.

All participants attending the conference will be required to complete anevaluation form in order to receive continuing education credit.
Questions? Please visit the Continuing Education tablelocated in the lobby.

25

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Notes

26

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Notes

27

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Notes

28

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Notes

29

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Notes

30

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Notes

31

9th Annual Amygdala, Stress and PTSD Conference: Bench to Bedside

Center for the Study of Traumatic Stress
Uniformed Services University of the Health Sciences
4301 Jones Bridge Road, Bethesda, MD 20814
Tel: 301-295-3294 | contact@amygdalaptsdconference.org
www.CSTSonline.org
32