In vivo measurement of presynaptic Zn2+ release during forebrain ischemia in rats

Youji Kitamura, Yasuhiko Iida, Jun Abe, Masaki Mifune, Fumiyo Kasuya, Masayuki Ohta, Kazuo Igarashi, Yutaka Saito, Hideo Saji

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)


Previous studies have suggested that during forebrain ischemia, considerable Zn2+ is released from synaptic vesicles of gultamatergic neuronal terminals and accumulates in hippocampal CA1 pyramidal neurons, leading to delayed neuronal death. However, since a time lag exists between the accumulation of Zn2+ and the occurrence of ischemia and there are conflicting reports about the amount of Zn2+ released, the level of released Zn2+ during ischemia in vivo is still unclear. In this study, we investigated the temporal change of extracellular Zn2+ in the hippocampal CA1 area using microdialysis and the accumulation of Zn 2+ in hippocampal CA1 neurons with TSQ staining in rats with a transient forebrain ischemia. The level of extracellular Zn2+ in the CA1 area increased transiently reaching a peak 15 min after occlusion, then decreased with time, returning to the basal level 15 min after reperfusion. In addition, at this peak, the level of extracellular Zn2+ was about twice the basal level. Assessment of the intracellular Zn2+ in hippocampal neurons with TSQ revealed that Zn2+ accumulate at 24 h, but not 0 and 6 h after ischemia. These results suggest that, although the synaptic vesicular Zn2+ is released into the synaptic cleft during ischemia in vivo, the amount of released Zn2 might not be so excessive, and it does not accumulate in hippocampal CA1 pyramidal neurons immediately after ischemia.

Original languageEnglish
Pages (from-to)821-823
Number of pages3
JournalBiological and Pharmaceutical Bulletin
Issue number4
Publication statusPublished - Apr 2006


  • Accumulation
  • Glutamate
  • Ischemia
  • Microdialysis
  • Zinc

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science


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