Glutamate neurotoxicity in cortical cell culture

@inproceedings{Choi1987GlutamateNI,
  title={Glutamate neurotoxicity in cortical cell culture},
  author={Dennis W. Choi and Margaret Maulucci-Gedde and Arnold R. Kriegstein},
  booktitle={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={1987}
}
The central neurotoxicity of the excitatory amino acid neurotransmitter glutamate has been postulated to participate in the pathogenesis of the neuronal cell loss associated with several neurological disease states, but the complexity of the intact nervous system has impeded detailed analysis of the phenomenon. In the present study, glutamate neurotoxicity was studied with novel precision in dissociated cell cultures prepared from the fetal mouse neocortex. Brief exposure to glutamate was found… Expand
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References

SHOWING 1-10 OF 59 REFERENCES
Synaptic release of excitatory amino acid neurotransmitter mediates anoxic neuronal death
  • S. Rothman
  • Biology, Medicine
  • The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1984
TLDR
Results provide convincing evidence that the synaptic release of excitatory transmitter mediates the death of anoxic neurons, and suggests new strategies that may be effective in preventing the devastating insults produced by cerebral hypoxia and ischemia in man. Expand
Investigations into the mechanism of excitant amino acid cytotoxicity using a well-characterized glutamatergic system
TLDR
In this insect glutamatergic system, when desensitization is prevented, activated glutamate receptors gate the influx of Ca2+ and Na2+ causing an ionic imbalance which results in cellular damage, which could account for at least some of the neurotoxic effects of amino acids in the vertebrate central nervous system. Expand
Duplication of biochemical changes of Huntington's chorea by intrastriatal injections of glutamic and kainic acids
TLDR
This work has injected 1 µl of either kainic acid or L-glutamic acid dissolved in isotonic saline directly into the extrapyramidal nuclei of rats, and found that injection into the striatum produced local enzymatic changes duplicating those reported in Huntington's chorea. Expand
Transport and Metabolism of Glutamate and Gaba in Neurons and Glial Cells
TLDR
It is undoubtedly correct that these amino acids can be taken up into presynaptic nerve endings through high-affinity transport processes and it is even possible to distinguish between these transport mechanisms employing inhibitors that have been shown to be selective for the transport carriers. Expand
The effects of glutamate and kainate on cell proliferation in retinal cultures.
  • A. Hyndman
  • Biology, Medicine
  • Investigative ophthalmology & visual science
  • 1984
TLDR
Glutamate appears to be a general retinal toxin, while the survival of immature neurons or glia is not affected by kainate, at the concentrations tested. Expand
Neurons containing NADPH-diaphorase are selectively resistant to quinolinate toxicity.
TLDR
The results support the hypothesis that the disease may be caused by excess exposure to quinolinate or some other endogenous N-methyl-D-aspartate agonist, and suggest neurons containing NADPH-d may have an unusual distribution of receptors for excitatory amino acids. Expand
Comparison of ibotenate and kainate neurotoxicity in rat brain: A histological study
TLDR
These findings, together with differences between the two toxins in the evolution of neuronal degeneration, appear to support previous suggestions that ibotenate and kainate exert their excitotoxic actions via different mechanisms. Expand
Chronic infusion of endogenous excitatory amino acids into rat striatum and hippocampus
TLDR
It appears, however, that these protective mechanisms can be overcome by extremely high local concentrations of glutamate or aspartate. Expand
Structure-activity relations for the neurotoxicity of kainic acid derivatives and glutamate analogues
TLDR
In both the retina and corpus striatum, dihydrokainate, N-acetylkainates and kainic acid dimethylester are at least 45 to 100-fold less toxic than kainate. Expand
Development of muscarinic receptor binding in spinal cord cell cultures and its reduction by glutamic and kainic acids.
TLDR
The findings suggest that 80% or more of muscarinic binding sites in the spinal cord cell cultures are on neurons and that the sensitivity of these neurons to the toxic action of glutamate increases with their maturation in vitro. Expand
...
1
2
3
4
5
...