Depletion of intracellular zinc from neurons by use of an extracellular chelator in vivo and in vitro.

Autor: Frederickson CJ; NeuroBioTex, Inc., Galveston, Texas 77550, USA. chris@neurobiotex.com, Suh SW, Koh JY, Cha YK, Thompson RB, LaBuda CJ, Balaji RV, Cuajungco MP
Jazyk: angličtina
Zdroj: The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society [J Histochem Cytochem] 2002 Dec; Vol. 50 (12), pp. 1659-62.
DOI: 10.1177/002215540205001210
Abstrakt: The membrane-impermeable chelator CaEDTA was introduced extracellularly among neurons in vivo and in vitro for the purpose of chelating extracellular Zn(2+). Unexpectedly, this treatment caused histochemically reactive Zn(2+) in intracellular compartments to drop rapidly. The same general result was seen with intravesicular Zn(2+), which fell after CaEDTA infusion into the lateral ventricle of the brain, with perikaryal Zn(2+) 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 Zn(2+) selectively.
Databáze: MEDLINE