Dendritic and mitochondrial changes during glutamate excitotoxicity

Sam M. Greenwood, Christopher N. Connolly

    Research output: Contribution to journalReview article

    88 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)891-898
    Number of pages8
    JournalNeuropharmacology
    Volume53
    Issue number8
    DOIs
    Publication statusPublished - Dec 2007

    Keywords

    • excitotoxicity
    • glutamate
    • dendrite injury
    • beading
    • mitochondrial dysfunction
    • dendrite remodelling
    • CEREBELLAR GRANULE CELLS
    • METHYL-D-ASPARTATE
    • ACUTE HIPPOCAMPAL SLICES
    • PERMEABILITY TRANSITION
    • RECEPTOR ACTIVATION
    • TRANSGENIC MICE
    • KAINIC ACID
    • IN-VIVO
    • MEDIATED EXCITOTOXICITY
    • NEURITIC DEGENERATION

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