Topical Review: Glutamate in Neurologic Diseases

@article{Bittigau1997TopicalRG,
  title={Topical Review: Glutamate in Neurologic Diseases},
  author={Petra Bittigau and Chrysanthy Ikonomidou},
  journal={Journal of Child Neurology},
  year={1997},
  volume={12},
  pages={471 - 485}
}
Excitotoxicity has been implicated as a mechanism of neuronal death in acute and chronic neurologic diseases. Cerebral ischemia, head and spinal cord injury, and prolonged seizure activity are associated with excessive release of glutamate into the extracellular space and subsequent neurotoxicity. Accumulating evidence suggests that impairment of intracellular energy metabolism increases neuronal vulnerability to glutamate which, even when present at physiologic concentrations, can damage… Expand
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References

SHOWING 1-10 OF 284 REFERENCES
Excitotoxicity and neurodegenerative diseases.
TLDR
The concept of increased neuronal vulnerability to excitotoxic injury establishes a link between slow neuronal degeneration and excitOToxicity and suggests that glutamate antagonists may prove beneficial in the treatment of chronic neurodegenerative diseases that have been resistant to therapy. Expand
Neurodegenerative disorders: clues from glutamate and energy metabolism.
TLDR
Experimental observations suggest that disturbed energy metabolism and glutamate may be involved in neuronal death leading to abiotrophic/neurodegenerative disorders in humans and, if so, glutamate antagonists or agents that improve energy metabolism may slow the degenerative process and offer a therapeutic approach for temporarily retarding the progression of these disabling disorders. Expand
Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses?
  • M. Beal
  • Biology, Medicine
  • Annals of neurology
  • 1992
TLDR
If defective mitochondrial energy metabolism plays a role in cell death in neurodegenerative disorders, potential therapeutic strategies would be to use excitatory amino acid antagonists or agents to bypass bioenergetic defects. Expand
Energy Failure, Glutamate and Neuropathology: Relevance to Neurodegenerative Disorders
TLDR
Observations indicate that glutamate may be involved in slow neuronal death leading to abiotrophic disorders and suggest the use of glutamate antagonists as potential neuroprotective agents to prevent or retard neuronal damage and death in relevant regions of the brain. Expand
A potential role for excitotoxins in the pathophysiology of spinal cord injury
TLDR
Findings indicate that NMDA antagonists may be beneficial in the treatment of traumatic spinal cord injury and extend the excitotoxin concept to central nervous system trauma. Expand
Oxidative stress, glutamate, and neurodegenerative disorders.
TLDR
Two broad mechanisms--oxidative stress and excessive activation of glutamate receptors--are converging and represent sequential as well as interacting processes that provide a final common pathway for cell vulnerability in the brain. Expand
Glutamate neurotoxicity in cortical cell culture
TLDR
Some neurons regularly survived brief glutamate exposure; these possibly glutamate-resistant neurons had electrophysiologic properties, including chemosensitivity to glutamate, that were grossly similar to those of the original population. Expand
Excitotoxic mechanisms of epileptic brain damage.
TLDR
It is found that the seizure-brain damage syndrome induced by cholinergic agents can be prevented by pretreatment with atropine and that the Syndrome induced by any of the above methods can be either prevented or aborted respectively by either pre- or posttreatment with diazepam. Expand
Excitatory amino acid neurotoxicity and neurodegenerative disease.
TLDR
In vivo and in vitro studies of the cytotoxicity of amino acids are reviewed and the contribution of such toxicity to acute and chronic neurodegenerative disorders is summarized. Expand
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