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Aurintricarboxylic Acid Protects Hippocampal Neurons from NMDA‐and Ischemia‐Induced Toxicity In Vivo
Author(s) -
RobertsLewis Jill M.,
Marcy Val R.,
Zhao Yonghua,
Vaught Jeffry L.,
Siman Robert,
Lewis Michael E.
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb03583.x
Subject(s) - aurintricarboxylic acid , programmed cell death , spectrin , hippocampal formation , calpain , neuroprotection , apoptosis , in vivo , ischemia , biology , microbiology and biotechnology , pharmacology , neuroscience , biochemistry , cell , medicine , enzyme , cytoskeleton
The polymeric dye aurintricarboxylic acid (ATA) has been shown to protect various cell types from apoptotic cell death, reportedly through inhibition of a calcium‐dependent endonuclease activity. Recent studies have indicated that there may be some commonalities among apoptosis, programmed cell death, and certain other forms of neuronal death. To begin to explore the possibility of common biochemical mechanisms underlying ischemia‐or excitotoxin‐induced neuronal death and apoptosis in vivo, gerbils or rats subjected to transient global ischemia or NMDA microinjection, respectively, received a simultaneous intracerebral infusion of ATA or vehicle. As a biochemical marker of neuronal death, spectrin proteolysis, which is mediated by activation of calpain I, was measured in hippocampus after 24 h. ATA treatment resulted in a profound reduction of both NMDA‐and ischemia‐induced spectrin proteolysis, consistent with the possibility of some common mechanism in apoptosis and other forms of neuronal death in vivo.