Abstract
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 100 mM 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 zincdeficient 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 th ee nhancement of exocytosis associated with affected Ca 2+ mobilization. The expression of GLT-1, a glial glutamate transporter, in the hippocampus was higher in zincdeficient 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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have