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J.Health Sci., 55(3), 405-412, 2009
High K+-induced Increase in Extracellular Glutamate in Zinc Deficiency and Endogenous Zinc Action
Atsushi Takeda,* Hiromasa Itoh,
Haruna Tamano, and Naoto Oku
Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Shizuoka 422-8526, Japan
To understand the physiological significance of endogenous zinc release under excess excitation in the hippocampus, in the present study, high K+-induced increase in extracellular glutamate and endogenous zinc action against its increase were examined in young rats fed a zinc-deficient diet for 2 weeks. When the ventral hippocampus was perfused by 100mM KCl, the extracellular concentration of glutamate was more increased in zinc-deficient rats than the control rats. Calcium orange signal in mossy fiber boutons was more increased in slices from zinc-deficient rats after delivery of tetanic stimuli (100 Hz, 5 sec) to the dentate granule cell layer. The decrease in FM4-64 signal, which is a measurement of exocytosis, in mossy fiber boutons was also enhanced in slices from zinc-deficient rats. These results suggest that the abnormal increase in extracellular glutamate in the hippocampus induced with high K+ in zinc deficiency is due to the enhancement of exocytosis associated with affected Ca2+ mobilization. The expression of GLT-1, a glial glutamate transporter, in the hippocampus was higher in zinc-deficient rats, suggesting that GLT-1 protein increased serves to maintain the basal concentration of extracellular glutamate, which was not different between the control and zinc-deficient rats. On the other hand, the increase in extracellular glutamate concentration induced with high K+ was enhanced in the presence of 1 mM CaEDTA, a membrane-impermeable zinc chelator, in both the control and zinc-deficient rats. It is likely that zinc released from glutamatergic neurons serves to suppress glutamate release under excess excitation in the hippocampus.
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