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 language | English (US) |
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Pages (from-to) | 1060-1064 |
Number of pages | 5 |
Journal | Neuroreport |
Volume | 21 |
Issue number | 16 |
DOIs | |
State | Published - Nov 17 2010 |
Externally published | Yes |
Keywords
- CA1
- hippocampal slice
- ischemia
- oxygen/glucose deprivation
- spreading depression
- zinc