Neuroscience 2002 Abstract
| Presentation Number: | 197.9 |
|---|---|
| Abstract Title: | Monitoring of neuronal intracellular free zinc in murine hippocampal slices exposed to oxygen-glucose deprivation. |
| Authors: |
Takata, T.*1
; Ouyang, Y.1
; Sheline, C. T.1
; Choi, D. W.1
1Neurology and Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Ischemia -- Cellular and molecular mechanisms |
| Session: |
197. Ischemia: cellular and molecular mechanisms III Poster |
| Presentation Time: | Sunday, November 3, 2002 1:00 PM-2:00 PM |
| Location: | Hall A2-B3 Y-11 |
| Keywords: | FuraZin-1, CaEDTA, ZnT3 KO mice |
Zinc toxicity has been postulated to contribute to selective neuronal death after transient global ischemia. We have modeled this injury mechanism in acutely-prepared adult rat hippocampal slices exposed to oxygen-glucose deprivation (Canzoniero L.M.T. et al. SFN abstract vol. 26:763,2000); neuronal death in this model is associated with an increase in intracellular zinc, and is reduced by the application of the extracellular chelator, CaEDTA.
We have now extended study of the oxygen-glucose deprivation-induced neuronal death to murine hippocampal slices, monitoring intracellular free zinc concentration with the ratiometric dye, FuraZin-1. The FuraZin-1 signal from both CA1 and CA3 areas showed a modest increase after 20 min of oxygen-glucose deprivation. Addition of 1mM CaEDTA to the bathing medium reduced the fluorescent signal from the CA3 area, but not the CA1 area. Next, we examined the slices from ZnT3 knockout mice, kindly provided by Richard Palmiter, that have little or no vesicular zinc in neuronal terminals. In slices prepared from these knockout mice, there was no increase of zinc signal from the CA3 area induced by oxygen-glucose deprivation. These results suggest that the zinc signal in CA3 is largely dependent upon the release of neuronal vesicular zinc stores.
We have now extended study of the oxygen-glucose deprivation-induced neuronal death to murine hippocampal slices, monitoring intracellular free zinc concentration with the ratiometric dye, FuraZin-1. The FuraZin-1 signal from both CA1 and CA3 areas showed a modest increase after 20 min of oxygen-glucose deprivation. Addition of 1mM CaEDTA to the bathing medium reduced the fluorescent signal from the CA3 area, but not the CA1 area. Next, we examined the slices from ZnT3 knockout mice, kindly provided by Richard Palmiter, that have little or no vesicular zinc in neuronal terminals. In slices prepared from these knockout mice, there was no increase of zinc signal from the CA3 area induced by oxygen-glucose deprivation. These results suggest that the zinc signal in CA3 is largely dependent upon the release of neuronal vesicular zinc stores.
Supported by NIH NINDS grant NS 30337, NS 32636 (DWC) and Japan Foundation for Aging and Health (TT)
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
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