Delayed application of aurintricarboxylic acid reduces glutamate‐induced cortical neuronal injury

Delayed application of aurintricarboxylic acid reduces glutamate‐induced cortical neuronal injury The non‐specific endonuclease inhibitor, aurintricarboxylic acid (ATA), attenuated glutamate‐induced destruction of cultured cortical neurons. In part, this protective effect likely reflected the ability of ATA to produce a slowly developing block of N‐methyl‐D‐aspartate receptor‐mediated inward whole cell current or increase in intracellular free Ca2+. However, ATA also attenuated a high K+‐induced increase in intracellular free Ca2+ in the presence of D‐aminophosphonovalerate, suggesting that ATA may have a more general effect on Ca2+ homeostasis. In addition, ATA attenuated glutamate neurotoxicity even if added up to 2 hr after completion of glutamate exposure, a time when glutamate antagonists or lipid peroxidation inhibitors are no longer neuroprotective. Involvement of apoptosis in this excitotoxic death is unlikely, as Southern blotting of genomic DNA revealed no evidence of fragmentation, and death was not prevented by inhibitors of RNA or protein synthesis. Most likely, ATA interferes with some key downstream consequences of excitotoxic glutamate receptor overactivation. © 1994 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neuroscience Research Wiley

Delayed application of aurintricarboxylic acid reduces glutamate‐induced cortical neuronal injury

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Abstract

The non‐specific endonuclease inhibitor, aurintricarboxylic acid (ATA), attenuated glutamate‐induced destruction of cultured cortical neurons. In part, this protective effect likely reflected the ability of ATA to produce a slowly developing block of N‐methyl‐D‐aspartate receptor‐mediated inward whole cell current or increase in intracellular free Ca2+. However, ATA also attenuated a high K+‐induced increase in intracellular free Ca2+ in the presence of D‐aminophosphonovalerate, suggesting that ATA may have a more general effect on Ca2+ homeostasis. In addition, ATA attenuated glutamate neurotoxicity even if added up to 2 hr after completion of glutamate exposure, a time when glutamate antagonists or lipid peroxidation inhibitors are no longer neuroprotective. Involvement of apoptosis in this excitotoxic death is unlikely, as Southern blotting of genomic DNA revealed no evidence of fragmentation, and death was not prevented by inhibitors of RNA or protein synthesis. Most likely, ATA interferes with some key downstream consequences of excitotoxic glutamate receptor overactivation. © 1994 Wiley‐Liss, Inc.

Journal

Journal of Neuroscience ResearchWiley

Published: May 1, 1994

References

  • Aurintricarboxylic acid rescues PC12 cells and sympathetic neurons from death caused by nerve growth factor deprivation: correlation with suppression of endonuclease activity
    Batistatou, Batistatou; Greene, Greene
  • Structure‐activity analysis of binding kinetics or NMDA receptor competitive antagonists: the influence of conformational restriction
    Benveniste, Benveniste; Mayer, Mayer
  • Excitotoxicity and the NMDA receptor
    Rothman, Rothman; Olney, Olney
  • Cell death: the significance of apoptosis
    Wyllie, Wyllie; Kerr, Kerr; Currie, Currie

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