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Journal of Histochemistry and Cytochemistry, Vol. 50, 1659-1662, December 2002, Copyright © 2002, The Histochemical Society, Inc.

ARTICLE

Depletion of Intracellular Zinc from Neurons by Use of an Extracellular Chelator In Vivo and In Vitro

Christopher J. Fredericksona, Sang W. Suha, Jae-Young Kohb, Yoo K. Chab, Richard B. Thompsonc, Christopher J. LaBudaa, Rengarajan V. Balajia, and Math P. Cuajungcod
a NeuroBioTex, Inc., Galveston, Texas
b National Creative Research Initiative Center for the Study of CNS Zinc, University of Ulsan College of Medicine, Seoul, Korea
c Department of Biochemistry, University of Maryland Medical School, Baltimore, Maryland
d Harvard Institute of Human Genetics, Harvard Medical School, Boston, and Massachusetts General Hospital, Molecular Neurogenetics Unit, Charlestown, Massachusetts

Correspondence to: Christopher J. Frederickson, NeuroBioTex, Inc., 101 Christopher Columbus Blvd., Galveston, TX 77550. E-mail: chris@neurobiotex.com

The membrane-impermeable chelator CaEDTA was introduced extracellularly among neurons in vivo and in vitro for the purpose of chelating extracellular Zn2+. Unexpectedly, this treatment caused histochemically reactive Zn2+ in intracellular compartments to drop rapidly. The same general result was seen with intravesicular Zn2+, which fell after CaEDTA infusion into the lateral ventricle of the brain, with perikaryal Zn2+ in Purkinje neurons (in vivo) and with cortical neurons (in vitro). These findings suggest either that the volume of zinc ion efflux and reuptake is higher than previously suspected or that EDTA can enter cells and vesicles. Caution is therefore warranted in attempting to manipulate extracellular or intracellular Zn2+ selectively. (J Histochem Cytochem 50:1659–1662, 2002)

Key Words: zinc, hippocampus, nitric oxide, TSQ, (N-(6-methoxy-8-quinolyl)- para-toluenesulfonamide), neurotoxicity, CaEDTA


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