Carl Faingold, PhD

Southern Illinois University

Carl Faingold, PhD, obtained his B.S. from the University of Illinois and his Ph.D. in Pharmacology from Northwestern University. He joined Southern Illinois University in 1972 as assistant professor and was promoted to full professor of Pharmacology in 1987. He received the University Distinguished Scholar award in 2009. He became chairman of the Department of Pharmacology in 1995 and professor of Neurology in 1993. Dr Faingold has published scholarly works in several fields, including epilepsy research, hearing research, pharmacology teaching, and alcoholism research. He has published more than 120 peer-reviewed scientific papers, and more than 40 book chapters and reviews. His publications and grants focus on the importance of neuronal networks in epileptic disorders (Faingold and Fromm, Drugs for Control of Epilepsy: Actions on Neuronal Networks Involved in Seizure Disorders, 1992 (CRC Press). He co-edited a book (Faingold and Blumenfeld, 2014), Neuronal Networks in Brain Function, CNS Disorders, and Therapeutics, San Diego, CA: Elsevier/ Academic Press, which proposed a new concept in understanding the actions of CNS drugs and stimulation therapies on disorders of the brain. Dr Faingold's most recent research has focused on an important area of epilepsy, sudden unexpected death in epilepsy (SUDEP). He and his colleagues have recently developed and published new models for human SUDEP in DBA/1 and DBA/2 mice that are allowing evaluation of potential preventive treatments for this devastating problem. This work has highlighted the importance of the neurotransmitters serotonin and adenosine in control of respiratory function by the brain, which appears to be abnormal in these models of SUDEP and in human SUDEP. Drugs that enhance the action of serotonin will block sudden death in this model. His most recent work has investigated the importance of specific subcortical brain structures in the susceptibility of this model to SUDEP, and the role of these structures as targets of drug action to prevent SUDEP. Further exPlenaryoration of this SUDEP model will hopefully yield possible agents for prevention of human SUDEP.

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