Journal
NEUROPHARMACOLOGY
Volume 53, Issue 8, Pages 891-898Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2007.10.003
Keywords
excitotoxicity; glutamate; dendrite injury; beading; mitochondrial dysfunction; dendrite remodelling
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Glutamate is the predominant excitatory neurotransmitter in the mammalian central nervous system (CNS) and is normally stored intracellularly. However, in instances of CNS injury or disease, increased concentrations of extracellular glutamate can result in the over-activation of ionotropic glutamate receptors and trigger neuronal cell death (termed excitotoxicity). Two early hallmarks of such neuronal toxicity are mitochondrial dysfunction (depolarisation, decreased ATP synthesis, structural collapse and potential opening of the permeability transition pore) and the formation of focal swellings (also termed varicosities/beads) along the length of the dendrites. In this review, we summarise current knowledge of the mechanisms that underlie these early excitotoxic events as well as the mechanisms that facilitate dendritic recovery following termination of the excitotoxic insult. (c) 2007 Elsevier Ltd. All rights reserved.
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