Carl Faingold, Ph.D.


    About me



    Research Interests and Specialties:

    The Faingold lab investigates brain function and how epilepsy, alcoholism, chronic pain, and anticonvulsants alter this function.  We use several techniques in our experiments, including neurophysiology, neuroanatomy, neuropharmacology, and neuroimaging in intact behaving animals to investigate these problems. The billions of neurons in the brain are organized into networks that are responsible for both normal and abnormal brain function. Epilepsy, alcoholism, and neuropathic pain all produce abnormal neuronal network function, involving brain areas that are capable of undergoing major operational changes due to neuroplasticity. Epilepsy is the most common neurological disorder of brain networks in man, and a major devastating consequence is sudden unexpected death in epilepsy (SUDEP). Alcoholism is a major health problem, and the neurobiology of alcohol withdrawal is poorly understood. Neuropathic pain involves abnormal responses to non-painful stimuli, and the brain mechanisms involved require further research. Current treatments do not adequately control these conditions. SUDEP in epilepsy patients involve breathing problems associated with seizures, and we are investigating a mouse SUDEP model and evaluating drugs that may be useful in SUDEP prevention. Another major goal of the lab is to understand brain mechanisms that produce seizures and to identify anticonvulsant drugs which prevent abnormal brain activity without affecting normal function. Many of these anticonvulsants are also effective in treating alcohol withdrawal and neuropathic pain.  To better understand network functions in health and disease, we evaluate neurotransmitters, which govern neuronal excitability by giving drugs that modify transmitter action. Brain surgery and computer-assisted single cell recording are methods we use to test the effects of drugs on brain network sites in conscious animals. The experiments involve animals with genetically-based epilepsy and animals subject to ethanol withdrawal or neuropathic pain. This research is identifying specific neuronal networks and specific neurotransmitters that are involved in these processes, which include GABA, glutamate, and serotonin. These substances are normal neurotransmitters, but their effects are altered in these brain disorders. Completion of these research goals will improve the understanding of normal and abnormal brain function and improve the treatment of these neurological disorders.

    Education & training

    Undergraduate Degree
    B.S. (Pharmacy); University of Illinois at Chicago, Chicago, IL
    Ph.D. (Pharmacology); Northwestern University, Chicago, IL


    Recent (from over 150 peer-reviewed journal articles reviews and book chapters)

    Faingold CL and Blumenfeld H, book editors. Neuronal Networks in Brain Function, CNS Disorders, and Therapeutics. San Diego, CA: Elsevier/Academic Press 2014

    Tupal, S. and Faingold, C.L. The amygdala to periaqueductal gray pathway: Plastic changes induced by audiogenic kindling and reversal by gabapentin. Brain Res. 1475:71-79, 2012.

    Faingold, C.L. Kommajosyula, S.P., Long, X., Plath, K., Randall, M. Serotonin and sudden death: Differential effects of serotonergic drugs on seizure-induced respiratory arrest in DBA/1 mice.  Epilepsy Behav. 37:198-203, 2014.

    Faingold, C.L., and Blumenfeld, H. Targeting Neuronal Networks with Combined Drug and Stimulation Paradigms Guided by Neuroimaging to Treat Brain Disorders. The Neuroscientist, 21(5) 460–47, 2015.

    Kommajosyula, S.P., Randall, M.E., Tupal, S., and Faingold, C.L., Alcohol withdrawal in epileptic rats — Effects on postictal depression, respiration, and death, Epilepsy & Behavior 64 (2016) 9–14.

    Faingold CL, Randall M, Zeng C, Peng S, Long X, Feng HJ, Serotonergic agents act on 5-HT3 receptors in the brain to block seizure-induced respiratory arrest in the DBA/1 mouse model of SUDEP.  Epilepsy Behav. 2016 Oct 12;64(Pt A):166-170. 

    Samineni, V.K, Premkumar, L.S., Faingold, C.L., Neuropathic pain induced enhancement of spontaneous and pain evoked neuronal activity in the periaqueductal gray that is attenuated by gabapentin, PAIN, 2017 (in press).


    Outstanding Scholar Award, Southern Illinois University, Carbondale, IL (2009)