Release of vesicular Zn2+ in a rat transient middle cerebral artery occlusion model

Abstract In the brain, Zn 2+ is stored in synaptic vesicles of a subgroup of glutamatergic nerve terminals. Although it has been reported that this Zn 2+ is released upon the excitation of nerves in vitro, there has been little study of the release of Zn 2+ during ischemia in vivo. Here, using brain microdialysis, the release of vesicular Zn 2+ was investigated in vivo. When the vesicular Zn 2+ was released into the synaptic cleft by a depolarizing stimulation achieved by perfusion with Ringer's solution containing high K + (100 mM KCl), a significant increase in the extracellular concentration of Zn 2+ could be detected by microdialysis. Then, we investigated the release of vesicular Zn 2+ in a rat transient middle cerebral artery occlusion model using microdialysis. Consequently, the extracellular Zn 2+ level in the cortex increased within 15 min of the start of occlusion and reached a peak at 30 min, which was about twice the basal level. After 30 min, it declined with time returning to the basal level 15 min after reperfusion, which was performed after 60 min of occlusion. The results suggest that vesicular Zn 2+ would be released into the synaptic cleft during brain ischemia in vivo.