期刊
JOURNAL OF NEUROSCIENCE
卷 27, 期 16, 页码 4253-4260出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0211-07.2007
关键词
astrocyte; global ischemia; glutamate transporter; hippocampus; mitochondria; oxidative stress
资金
- NIGMS NIH HHS [GM49831, R01 GM049831] Funding Source: Medline
- NINDS NIH HHS [NS053898, R01 NS053898, R01 NS053898-02, NS014543, P01 NS014543, NS037520, P50 NS014543, P01 NS037520] Funding Source: Medline
Transient global ischemia, as with cardiac arrest, causes loss of CA1 hippocampal neurons 2-4 d later, whereas nearby dentate gyrus (DG) neurons are relatively resistant. Whether differential astrocyte vulnerability in ischemic injury contributes to CA1 neuronal death is uncertain. Here, we find that CA1 astrocytes are more sensitive to ischemia than DG astrocytes. In rats subjected to transient forebrain ischemia, CA1 astrocytes lose glutamate transport activity and immunoreactivity for GFAP, S100 beta, and glutamate transporter GLT-1 within a few hours of reperfusion, but without astrocyte cell death. Oxidative stress may contribute to the observed selective CA1 changes, because CA1 astrocytes show early increases in mitochondrial free radicals and reduced mitochondrial membrane potential. Similar changes were not observed in DG astrocytes. Upregulation of GLT-1 expression in astrocytes with ceftriaxone protected CA1 neurons from forebrain ischemia. We suggest that greater oxidative stress and loss of GLT-1 function selectively in CA1 astrocytes is central to the well known delayed death of CA1 neurons.
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