Dr. Abel received a B.S. in Biology and a B.A. in Psychology from Oakland University in 1974. He received his M.S. in Physiology from Wayne State University in 1977, and his Ph.D. in Neurobiology from The University of Texas in 1981. He was an Adjunct Assistant Professor in the Department of Psychology of City College, City University of New York, and a Senior Research Biochemist and Team Leader in the Molecular Neurobiology Group of the Department of CNS Biology at Lederle Laboratories until 1990, when he joined the faculty of FUHS/The Chicago Medical School. He is a member of the editorial board of Metabolic Brain Disease, and an ad hoc member of the Minority Biomedical Research Support (MBRS) Neuroscience/Pharmacology Review Panel, NIGMS, NIH. He is a member of the Society For Neuroscience, American Association of Anatomists, Sigma Xi, and American Association for the Advancement of Science. Dr. Abel's major funding sources have been the National Institute on Drug Abuse at NIH and the American Heart Association. He has been course director for Clinical Anatomy, Speaker of the Academic Assembly, and is currently the Chair of the Educational Affairs Committee.

Research

Dr. Abel's research addresses the role of the central nervous system inhibitory neurotransmitter, GABA, and it's receptors, in the molecular and behavioral responses to repeated cocaine administration.

The GABAA receptor comprises several protein subunits, each of which is translated from a specific mRNA. Multiple subtypes exist for each subunit, and there is a heterogeneous distribution of these messages in the CNS. The assembled membrane-bound receptor forms a ligand-gated chloride ion channel, that contains domains for the binding of a number of pharmacological agents, including benzodiazepines, barbiturates, and neurosteroids, in addition to GABA itself. The allosteric interactions of these sites provide for a dynamic system that is modulated in various ways. Using radioligand binding and molecular biological techniques, the involvement of the GABAA receptor in cocaine-induced behavioral sensitization and kindled seizures is studied. Changes are identified in the expression of GABAA receptor subunits in the hippocampus. In cocaine-kindled seizures, in particular, the changes are long-lived, and parallel the behavioral responses to cocaine.

Dr. Abel's laboratory has recently been investigating the role of the GABAA receptor in response to repeated cocaine administration. The expression of this metabotropic receptor also changes during the kindling process.

Together, these data suggest that GABA system alterations are part of the neurobiological plasticity underlying cocaine-kindled seizures. Cocaine abuse remains a significant concern for our society, and cocaine-related seizures are a major component of repeated use. This research will help determine the processes responsible for these effects.

Contact information

Marc S. Abel, Ph.D.
Department of Cell Biology and Anatomy
The Chicago Medical School
3333 Green Bay Road
North Chicago, Illinois 60064

Email: marc.abel@rosalindfranklin.edu
Phone: (847) 578-3236
Fax: (847) 578-3253