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You are here: FRIAS Fellows Fellows 2017/18 Prof. Dr. med. Thomas J. Feuerstein

Prof. Dr. med. Thomas J. Feuerstein

University Hospital Freiburg
Internal Senior Fellow
October 2013 - July 2014

Phone + 49 761 270 52800


My studies of medicine at the University of Freiburg, Germany, concluded with a dissertation at the Institute of Medical Statistics and Documentation (Topic: Simulation studies of the genetic correlation coefficient). After my - then mandatory - military service as staff physician I continued my postdoctoral work at the State Psychiatric Hospital Reichenau and the Neurological University Hospital Freiburg. Due to my strong interest in neuro- and psychopharmacology, I transferred to the Institute of Pharmacology at the University of Freiburg and specialized first in pharmacology and toxicology.
I then returned to the Neurological University Hospital to complete my training as a neurologist and qualified for my state doctorate (Habilitation) in 1988. I was awarded the Constance Medical Sponsorship in 1989.
From 1989 to 1994, I worked as Head of Department, Clinical Research CNS, at the pharmaceutical firm of Goedecke AG / Parke-Davis (Freiburg and Ann Arbor, Michigan).
In 1994, I accepted the offer to became University Professor and was appointed head of the Section of Clinical Neuropharmacology, Neurocenter of the University Hospital Freiburg.
In 1995, I ranked third for the position of Chair Pharmacology, University of Dresden. In 1996 I ranked second for the same position at the University of Göttingen and, after the lead candidate declined, was given the first position.
My current research interests are focused on a focal neocortical epilepsy model in the rat to test local anti-epileptic therapies and transporter-mediated selective GABA release as an endogenous anti-seizure mechanism.


Selected Publications

  • Feuerstein TJ, Limberger N (1999) Mathematical analysis of the control of neurotransmitter release by presynaptic receptors as a supplement to experimental data. Naunyn-Schmiedeberg´s Arch Pharmacol 359:349-359
  • Stefan H, Feuerstein TJ (2007) Novel anticonvulsant drugs. Pharmacol Ther 113:165-183
  • Feuerstein TJ (2008) Presynaptic receptors for dopamine, histamine and serotonin.Handb Exp Pharmacol 184:289-338
  • Feuerstein TJ, Kammerer M, Lücking CH, Moser A (2011) Selective GABA release as a mechanistic basis of high frequency stimulation used for the treatment of neuropsychiatric diseases. Naunyn-Schmiedberg´s Arch Pharmacol 384:1-20
  • Rassner MP, van Velthoven-Wurster V, Ramantani G, Feuerstein TJ (2013) Altered transporter-mediated neocortical GABA release in Rasmussen encephalitis. Epilepsia 54(3):e41–e44


FRIAS Research Project

Transporter-mediated GABA release as endogenous anti-seizure defense mechanism

The human brain is predisposed to epileptic seizures under certain circumstances. Fortunately, endogenous anti-seizure mechanisms usually prevent such seizures. One of the most important mechanisms in this regard is transporter-mediated GABA release. The notion that synaptic transmission occurs solely by exocytosis is definitely not the case for GABA neurons. Transporter-mediated GABA release happens, for instance, when neurons are robustly depolarized due to repetitive influx of Na+ as occurs during epileptic seizures.

We characterized veratridine-evoked 3H-GABA release from human neocortical synaptosomes as caused solely by transporter reversal due to both depolarization and increased cytosolic Na+ ([Na+]i). Surprisingly, removal of extracellular Ca2+ ([Ca2+]e) increased this release, most probably by activating the synaptosomal Na+/Ca2+ exchanger (NCX) which further elevated [Na+]i and thus enhanced veratridine-induced transporter reversal. Increased GABA release due to decreased [Ca2+]e may counteract paroxysmal activity as lowering [Ca2+]e can induce spreading epileptiform activity.

My FRIAS project will investigate this anti-seizure defense mechanism in synaptosomes and in slices of human and rat neocortex. Methods are synaptosomal GABA release and patch-clamp analysis of pyramidal cells and GABAergic interneurons. The pre- and postsynaptic NCX will be analyzed at different [Ca2+]e to determine whether NCX modulation provides an antiepileptic target of possible clinical relevance. Specifically, a NCX-activating drug may offer a new anticonvulsant mechanism having a favorable side effect profile; i.e., this drug would selectively enhance (quasi-physiologically) an endogenous antiepileptic process, even more so when applied locally to ameliorate a seizure focus, yet not alter peripheral processes (e.g., cardiovascular).