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Cited by 528

Molecular mechanisms of glutamate-dependent neurodegeneration in ischemia and traumatic brain injury

Arundine, M., Tymianski, M.·2004·Cellular and Molecular Life Sciences (CMLS)
DOI 10.1007/s00018-003-3319-x
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Abstract

Stroke and neurotrauma mediate neuronal death through a series of events that involve multiple interdependent molecular pathways. It has been suggested that these pathways are triggered following elevations in extracellular excitatory amino acids, primarily glutamate [1]. This report outlines mechanisms involving glutamate-mediated excitotoxicity with specific focus on (i) the role of Ca(2+) in neurotoxicity, (ii) The concept of 'source specificity' of neurotoxicity, (iii) the role of the ionotropic N-methyl-D-aspartate (NMDA)-subtype glutamate receptor and its associated submembrane molecules that may give rise to signaling specificity in excitotoxicity and (iv) the role of glutamate-mediated free-radical generation and associated cell death pathways. We also highlight a novel, peptide-based approach for uncoupling NMDA receptors from excitotoxicity in the rat central nervous system subjected to focal ischemia, thereby reducing stroke infarct volume and improving neurological functioning.

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Crossref · 10.1007/s00018-003-3319-x

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  • These mechanisms range from inflammatory and glutamate excitotoxicity pathways, which increase metabolic demands of neurons and microglia, to oxidative stress pathways that may impact mitochondrial function.

    “They range from inflammatory and glutamate excitotoxicity pathways (57;58), which increase the metabolic demands of neurons and microglia, to oxidative stress pathways that may impact mitochondrial function (59).”

    From Association of ALS with head injury, cigarette smoking and APOE genotypes (2010) · cites this paper as [58]

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Authors
Arundine, M., & Tymianski, M.
Venue
Cellular and Molecular Life Sciences (CMLS)
Publisher
Springer Science and Business Media LLC
Published
2004-03-01
Volume
61
Issue
6
Pages
657-668
ISSN
  • 1420-682X
  • 1420-9071
DOI
10.1007/s00018-003-3319-x
Cited by
528
References
5
Licence
www.springer.com/tdm (tdm)

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