Lech Kiedrowski received his Ph.D. degree in the Natural Sciences (Biochemistry) in 1989 from the Polish Academy of Sciences (Nencki Institute of Experimental Biology, Warsaw). He performed postdoctoral studies (nitric oxide synthase activation in cultured neurons) at the Fidia-Georgetown Institute for the Neurosciences, directed by Dr. Erminio Costa, from 1989 to 1994. In 1994 Dr. Kiedrowski transferred to the Center for Neuropharmacology in the Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY, where he started to investigate the relationship between the glutamate-induced decline in mitochondrial membrane potential and neuronal death. Since joining the University of Illinois at Chicago in 1996 as an Assistant Professor of Pharmacology in Psychiatry, he has continued to study the mechanisms of excitotoxicity, in particular the effects of the NMDA-induced K+ efflux on plasma membrane potential, mitochondrial Ca2+ load, cytoplasmic pH, and neuronal viability. In 1998 Dr. Kiedrowski received a First Independent Research Award and Transition from the National Institute of Neurological Disorders and the Stroke Division of the National Institutes of Health in support of his research project entitled: "K+ efflux: Role in Ca2+ Homeostasis and Excitotoxicity."

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Representative Publications

Kiedrowski L. The difference between mechanisms of kainate and glutamate excitotoxicity in vitro: Osmotic lesion versus mitochondrial depolarization. (1998) Restor. Neurol. Neurosci. 12: 71-79.

Kiedrowski L. (1999) Elevated extracellular K+ concentrations inhibit N-methyl-D-aspartate- induced Ca2+ influx and excitotoxicity. Mol. Pharmacol. 56: 737-743.

Kiedrowski L. (1999) N-methyl-D-aspartate excitotoxicity: relationships among plasma membrane potential, Na+/ Ca2+ exchange, mitochondrial Ca2+ overload, and cytoplasmic concentrations of Ca2+, H+, and K+. Mol. Pharmacol. 56: 619-32.

Kiedrowski L. and Mienville J.-M. (2001) Kainate-induced K+ efflux and plasma membrane depolarization in cultured cerebellar granule cells. NeuroReport. 12: 59-62.

Kiedrowski L. (2001) Repolarization of the plasma membrane shapes NMDA-induced cytosolic [Ca2+] transients. NeuroReport. 12: 3579-3582.

Kiedrowski L., Czyż A., Li X.-F. and Lytton J. (2002) Preferential expression of plasmalemmal K-dependent Na/Ca exchangers in neurons versus astrocytes. NeuroReport 13: 1529-1532.

Kiedrowski L. and Czyż A. (2002) Mitochondria buffer sodium-dependent Ca2+ influx in cultured cerebellar granule cells. Ann N Y Acad Sci 976, 413-417.

Czyż A., Baranauskas G., Kiedrowski L. (2002) Instrumental role of Na+ in NMDA excitotoxicity in glucose-deprived and depolarized cerebellar granule cells. J. Neurochem. 81: 379-389.

Czyż A. and Kiedrowski L. (2002) In depolarized and glucose-deprived neurons, Na+ influx reverses plasmalemmal K-dependent and K-independent Na/Ca exchange and contributes to NMDA excitotoxicity. J. Neurochem. 83, 1321-1328.

Czyż A. and Kiedrowski L. (2003) Inhibition of plasmalemmal Na+/Ca2+ exchange by mitochondrial Na+/Ca2+ exchange inhibitor 7-chloro-5-(2-chlorophenyl)-1,5-dihydro-4,1-benzothiazepin-2(3H)-one (CGP-37157) in cerebellar granule cells. Biochem Pharmacol. 66, 2409-2411.

Kiedrowski L., Czyż A., Baranauskas G., Li X-F., Lytton J., (2004) Differential contribution of plasmalemmal Na+/Ca2+ exchange isoforms to sodium-dependent calcium influx and NMDA excitotoxicity in depolarized neurons. J. Neurochem. 90, 117-128.

Kiedrowski L. (2004) High activity of K+-dependent plasmalemmal Na+/Ca2+ exchangers in hippocampal CA1 neurons. NeuroReport, 15, 2113-2116.