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Review
. 2004 Mar;61(6):657-68.
doi: 10.1007/s00018-003-3319-x.

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

M Arundine  1 , M Tymianski
Affiliations
Review

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

M Arundine et al. Cell Mol Life Sci. 2004 Mar.

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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