Zn2+ chelation improves recovery by delaying spreading depression-like events

Russell E. Carter, John H. Weiss, C. William Shuttleworth

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

We earlier reported that Zn2+ chelation improved recovery of synaptic potentials after transient oxygen and glucose deprivation in brain slices. Such an effect could be because of reduced accumulation of Zn 2+ in postsynaptic neurons, or could also be due to prevention of the onset of spreading depression-like events. A combination of optical and electrical recording was used here to show that Zn2+ chelation is effective because it delays spreading depression-like events. If the duration of oxygen/glucose deprivation was sufficient to generate a spreading depression-like event, irrecoverable Ca2+-dependent loss of synaptic potentials occurred, regardless of Zn2+ availability. These results identify a key mechanism underlying protective effects of Zn2+ chelation, and emphasize the importance of evaluating spreading depression-like events in studies of neuroprotection.

Original languageEnglish (US)
Pages (from-to)1060-1064
Number of pages5
JournalNeuroreport
Volume21
Issue number16
DOIs
StatePublished - Nov 17 2010
Externally publishedYes

Keywords

  • CA1
  • hippocampal slice
  • ischemia
  • oxygen/glucose deprivation
  • spreading depression
  • zinc

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