Ted Abel
Professor, Dept of Biology

Genetics and Gene Regulation Program

Address

204G Carolyn Lynch Labs
433 S. University Ave.
Philadelphia . PA . 19104

Office tel.: 215 898-5614
Lab tel.: 215 898-3100
Fax: 215 898-8780
E-mail: abele@sas.upenn.edu

Link(s)

Ted Abel at the Dept of Bio

Education

Swarthmore College, B.A. (Chemistry), 1985

University of Cambridge, Christ’s College, M.Phil. (Biochemistry), 1987

Harvard University, Ph.D. (Biochemistry and Molecular Biology), 1993

College of Physicians and Surgeons, Columbia University, Postdoctoral Fellow, (Neuroscience),1997

Research Interests

• The molecular basis of synaptic plasticity, learning and memory
• The molecular basis of sleep/wake regulation

Key words: Memory storage; synaptic plasticity; long-term potentiation; behavior; sleep/wake states; genetically modified mice.

Description of Research

Synaptic plasticity, the change in the strength of neuronal connections in the brain, is thought to underlie memory storage and may play a crucial role in a variety of neurological and mental disorders, including mental retardation, Alzheimer’s disease and depression. The goal of much of our research is to use transgenic mice to explore the molecular basis of synaptic plasticity and memory storage. Recently, we have extended our studies of genetically modified mice to examine the role of specific signal transduction pathways in sleep/wake regulation.

Selected Publications

Bucan, M. and Abel, T. (2002). The mouse: Genetics meets behavior. Nature Reviews Genetics, 3:114-123.

Graves, L., Heller, E., Pack, A. and Abel, T. (2003). Sleep deprivation selectively impairs memory consolidation for contextual fear conditioning. Learning & Memory, 10: 168-176.

Graves, L., Hellman, K., Veasey, S., Blendy, J. A., Pack, A. and Abel, T. (2003). Genetic evidence for a role of CREB in sustained cortical arousal. Journal of Neurophysiology, 90: 1152-1159.

Lattal, K. M. and Abel, T. (2004). Behavioral impairments caused by injections of the protein synthesis inhibitor anisomycin after contextual retrieval reverse with time. Proceedings of the National Academy of Sciences 101: 4667-4672.

Wood, M. A., Kaplan, M. P., Park, A., Blanchard, E. J., Oliveira, A. M. M., Lombardi, T. L. and Abel, T. (2005). Transgenic mice expressing a truncated form of CREB-binding protein (CBP) exhibit deficits in hippocampal synaptic plasticity and memory storage. Learning & Memory 12: 111-119.

Search PubMed for more articles

Lab

Rotation Projects

1. Molecular Mechanisms of Memory Storage.
   One of the challenges in the study of signal transduction pathways in neurons is to understand the way in which signals are restricted to subcellular compartments and how different signaling pathways interact. To explore these issues, we are investigating the role of A kinase anchoring proteins (AKAPs) in learning and synaptic plasticity. AKAPs localize PKA to specific subcellular locations and assemble PKA into signaling modules that include phosphodiesterases, phosphatases, ion channels and receptors. A truncated form of one AKAP, Ht31, has been used as an inhibitor capable of blocking the interactions between PKA and other AKAPs. To study the role of PKA localization via interactions with AKAPs in learning and memory, we have generated conditional transgenic mice expressing a truncated form of Ht31 in neurons within the forebrain using the CaMKIIa promoter and the tetracycline regulatory system. We are examining learning and memory as well as synaptic plasticity in these transgenic mice to characterize the role of A kinase anchoring in hippocampal and amygdala function.
2. Temporal Regulation of Gene Expression.
   Inducible systems are crucial for determining if the phenotype observed in adult animals is due to acute expression of the transgene or due to an indirect effect of the transgene on developmental processes. Such regulation may be achieved by combining regionally restricted promoters with the tetracycline-inducible system. This system currently works most effectively by using the tetracycline trans-activator so that expression is shut off by the addition of the tetracycline analog doxycycline, a process that requires continuous treatment with doxycycline. We are currently using this system to control the timing of expression of the R(AB) transgene. One of our goals is to devise ways to modify this system so that inducible activation can be achieved efficiently in vivo. Combining regionally restricted and inducible gene expression will provide a more direct connection between behavioral deficits and synaptic plasticity in defined brain regions and will enable us to define precisely the role of PKA in memory acquisition, consolidation and retrieval.
3. The Identification of Genes Induced During Long-Term Memory Storage.
   One of the characteristics that distinguishes long-term memory storage from short-term processes is that long-term memory is sensitive to inhibitors of RNA and protein synthesis. The identification of the genes and proteins that are induced during long-term memory storage is a central problem in the field. Because R(AB) transgenic mice have selective long-term memory deficits, they provide an ideal opportunity to identify genes whose expression is induced or suppressed during learning. We are using a variety of molecular techniques to identity these genes.

Lab personnel:

Marcelo Wood, postdoctoral fellow
Michael Kaplan, postdoctoral fellow
Michele Kelly, postdoctoral fellow
Ted Huang (Neuroscience), graduate student
Conor McDonough (Neuroscience), graduate student
Ana Oliviera, graduate student
Chris Vecsey (Neuroscience), graduate student
Michael Esposito, undergraduate student