Ted Abel, Ph.D.
MIND Institute Distinguished Lecturer Series – May 18, 2016
Biographical Information
Ted Abel, Ph.D., is the Brush Family Professor of Biology and Director of the Biological Basis of
Behavior Program at the University of Pennsylvania where he also directs a Graduate Training
Program in Behavioral and Cognitive Neuroscience. His research focuses on the molecular
mechanisms of memory storage and the molecular basis of neurodevelopmental and psychiatric
disorders, examining the role of signaling pathways as well as transcriptional and epigenetic
regulation of gene expression. He has been a pioneer in the use of molecular and genetic
approaches to define how neural circuits mediate behavior, including identifying the molecular
impact of sleep deprivation on neuronal function. Dr. Abel has over 20 years of experience creating
and analyzing genetically modified mouse lines to study the basis of neurodevelopmental and
psychiatric disease at the behavioral, molecular, biochemical and electrophysiological level.
ogy
Dr. Abel was an undergraduate at Swarthmore College, receiving a B.A. in Chemistry in 1985. After
Swarthmore, Dr. Abel attended the University of Cambridge (Christ’s College) as a Marshall Scholar,
receiving an M. Phil. in Biochemistry and working with Dr. R. Tim Hunt on the cloning of cyclin. Dr.
Abel then moved to Harvard University to work with Dr. Tom Maniatis on transcriptional regulation
during Drosophila development as a National Science Foundation graduate fellow.
After receiving his Ph.D. in Biochemistry and Molecular Biology in 1993 from Harvard University, Dr.
Abel moved to the College of Physicians and Surgeons at Columbia University to do his postdoctoral
work with Dr. Eric Kandel on genetic approaches to study the role of protein kinase A in neuronal
function. During his postdoctoral research, Dr. Abel received a fellowship from the Damon RunyonWalter Winchell Cancer Research Fund and a young investigator award from the National Alliance
for Research on Schizophrenia and Depression (NARSAD). In 1998, Dr. Abel joined the Biology
Department at the University of Pennsylvania as an Assistant Professor. As an independent
investigator, Dr. Abel has received a John Merck Scholars Award, a David and Lucile Packard
Fellowship in Science and Engineering and a Research Grant from the Human Frontiers Science
Program. In 1999, Dr. Abel received a Young Investigator Award from the Intellectual and
Developmental Disabilities Research Center at the Children’s Hospital of Philadelphia. In 2000, he
received the Daniel X. Freedman Award from NARSAD for outstanding research by a NARSAD
young investigator. Dr. Abel’s accomplishments in undergraduate teaching, research and advising
were recognized when he was named Biological Basis of Behavior Society Professor of the Year and
selected as the recipient of the School of Arts and Sciences Dean’s Award for Mentorship of
Undergraduate Research. In 2012, Dr. Abel was elected as a Fellow of the American College of
Neuropsychopharmacology. Dr. Abel has co-authored over 150 scientific papers, which have been
published in journals that include Nature, Science, Cell, Neuron, Journal of Clinical Investigation,
Proceedings of the National Academy of Sciences and the Journal of Neuroscience.
Presentation Abstract (4:30pm presentation)
Male-specific deficits in mouse models of autism
Neurodevelopmental disorders, including autism spectrum disorders (ASD), are highly male
biased, but the underpinnings of this are unknown. Striatal dysfunction has been strongly
implicated in the pathophysiology of neurodevelopmental disorders, raising the question of
whether there are sex differences in how the striatum is impacted by genetic risk factors
linked to neurodevelopmental disorders. We have identified male-specific deficits in striatal
function important to reward learning in a mouse model of 16p11.2 hemideletion, a genetic
mutation that is strongly associated with risk of neurodevelopmental disorders, particularly
autism and ADHD. We find that male, but not female, 16p11.2 deletion animals show
impairments in reward-directed learning and maintaining motivation to work for rewards.
Male, but not female, deletion animals overexpress mRNA for dopamine receptor 2 and
adenosine receptor 2a in the striatum, markers of medium spiny neurons signaling via the
indirect pathway, associated with behavioral inhibition. Despite equivalent effects in males
and females on the mRNA levels of genes located within the 16p11.2 region in the striatum,
including the kinase ERK1, hemideletion males show increased activation in the striatum for
ERK1 at baseline and in response to sucrose, a signaling change associated with decreased
striatal plasticity. In contrast, we find that hemideletion females show increased protein for
ERK1 as well as the related kinase ERK2, and no change in phosphorylation either at
baseline or in response to sucrose. These data indicate male-specific vulnerability in the
mechanisms regulating intracellular signaling in the brain as a result of a genetic lesion.
Interestingly, our work indicates that other mouse models of autism also show deficits in
reward learning, suggesting this as a common behavioral endophenotype of models of
autism.