RESEARCH INTERESTS

Research in my laboratory is focused on communication between neurons in the hippocampus, a brain region where epileptic seizures often start. This communication, called synaptic transmission, may be abnormal in epilepsy, and it is targeted by many antiepileptic medications. Much evidence supports the hypothesis that inhibitory synaptic transmission in particular is abnormal in epilepsy, making it less effective in counterbalancing excitation. In my laboratory, we use electrophysiological techniques to study how inhibitory synaptic transmission is regulated normally to maintain a precise balance of excitation and inhibition, thus preventing hyperexcitability and seizures. One major interest of my lab is the role of metabolism of the brain’s major inhibitory neurotransmitter, g-aminobutyric acid or GABA, in the regulation of inhibitory synaptic transmission.

SELECTED PUBLICATIONS:

Dzhala, V., Talos, D., Sdrulla, D., Brumback, A., Mathews, G.C., Benke, T., Delpire, E., Jensen, F. and Staley, K. NKCC1 transporter facilitates seizures in the developing brain. Nature Medicine, in press.

Mathews, G C, Diamond, J S. Neuronal glutamate uptake Contributes to GABA synthesis and inhibitory synaptic strength. J Neurosci, 23(6), 2040-8, 2003.

Silverman, I E, Restrepo, L, Mathews, G C. Poststroke seizures. Arch Neurol, 59(2), 195-201, 2002.

Mathews, G C, Bolos-Sy, A M, Covey, D F, Rothman, S M, Ferrendelli, J A. Physiological comparison of alpha-ethyl-alpha-methyl-gamma-thiobutyrolactone with benzodiazepine and barbiturate modulators of GABAA receptors. Neuropharmacology, 35(2), 123-36, 1996.

Holland, K D, Mathews, G C, Bolos-Sy, A M, Tucker, J B, Reddy, P A, Covey, D F, Ferrendelli, J A, Rothman, S M. Dual modulation of the gamma-aminobutyric acid type A receptor/ionophore by alkyl-substituted gamma-butyrolactones. Mol Pharmacol, 47(6), 1217-23, 1995.

Mathews, G C, Bolos-Sy, A M, Holland, K D, Isenberg, K E, Covey, D F, Ferrendelli, J A, Rothman, S M. Developmental alteration in GABAA receptor structure and physiological properties in cultured cerebellar granule neurons. Neuron, 13(1), 149-58, 1994.

Blazynski, C, Woods, C, Mathews, G C. Evidence for the action of endogenous adenosine in the rabbit retina: modulation of the light-evoked release of acetylcholine. J Neurochem, 58(2), 761-7, 1992.

Gregory C. Mathews, M.D., Ph.D.
Assistant Professor of Neurology
Epilepsy Division
6140 MRB III
465 21st Avenue South
Nashville TN 37232-8552
Phone: 615-322-5979
Fax: 615-322-5517

     
 
     

Faculty>
Gregory Mathews, M.D., Ph.D., Assistant Professor of Neurology

BIOGRAPHICAL SKETCH

Dr. Mathews received his B.S. degree from Georgetown University in 1989, and his M.D. and Ph.D. degrees from Washington University in St. Louis in 1996. He completed a residency in Neurology and a fellowship in Clinical Neurophysiology with emphasis on epilepsy at Johns Hopkins Hospital. After his fellowship he engaged in post-doctoral research training with Dr. Jeffrey S. Diamond at the National Institute of Neurological Disorders and Stroke.

In 2002, he was appointed to the faculty in the Department of Neurology at Johns Hopkins, and joined the faculty at Vanderbilt in July 2003. His research laboratory is working to better understand inhibitory synaptic transmission in the brain. He is board-certified in Neurology and in Clinical Neurophysiology. Dr. Mathews sees patients with epilepsy at the Vanderbilt Clinic and in Vanderbilt University Hospital’s Epilepsy Monitoring Unit.


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