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. 2000 Sep;106(6):723-31.
doi: 10.1172/JCI11003.

Brain tissue responses to ischemia

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Brain tissue responses to ischemia

J M Lee et al. J Clin Invest. 2000 Sep.
No abstract available

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Figure 1
Figure 1
Schematic of mechanisms implicated in ischemia-induced neuronal death (in red) and the development of ischemic tolerance (in blue) in the brain. During ischemia, glutamate is released into the synaptic cleft and activates NMDA receptors, increasing calcium entry. Calcium activates multiple pathways, promoting cellular injury via the generation of oxygen and NO radicals and the activation of catabolic enzymes. Sublethal insults may induce cytoprotective tolerance, in large part through similar NMDA receptor– and calcium-mediated pathways. Contributing prominently to the development of ischemic tolerance may be alterations in nerve terminals that increase release of GABA and reduce release of glutamate. GABA likely acts both presynaptically through GABAB receptors (and G-proteins) to decrease glutamate release and postsynaptically through GABAA receptors (and the gating of Cl channels to counter membrane depolarization and to limit calcium entry).

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References

    1. Choi DW. Glutamate neurotoxicity and diseases of the nervous system. Neuron. 1988;1:623–634. - PubMed
    1. Albers GW, Goldberg MP, Choi DW. N-methyl-D-aspartate antagonists: ready for clinical trial in brain ischemia? Ann Neurol. 1989;25:398–403. - PubMed
    1. Buchan AM. Do NMDA antagonists protect against cerebral ischemia: are clinical trials warranted? Cerebrovasc Brain Metab Rev. 1990;2:1–26. - PubMed
    1. Lee JM, Zipfel GJ, Choi DW. The changing landscape of ischaemic brain injury mechanisms. Nature. 1999;399:A7–A14. - PubMed
    1. Kerchner, G.A., Canzoniero, L.M.T., Yu, S.P., Ling, C., and Choi, D.W. 2000. Zinc current is mediated by voltage-gated calcium channels and enhanced by extracellular acidity in mouse cortical neurons. J. Physiol. In press. - PMC - PubMed

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