Homeostasis of glutamate in brain fluids: An accelerated brain-to-blood efflux of excess glutamate is produced by blood glutamate scavenging and offers protection from neuropathologies

V. I. Teichberg, K. Cohen-Kashi-Malina, I. Cooper, A. Zlotnik

    Research output: Contribution to journalReview articlepeer-review

    108 Scopus citations

    Abstract

    l-Glutamate (Glu) homeostasis in brain extracellular fluids and its maintenance at low micromolar concentrations in the face of the extremely high Glu concentrations present in brain cells and synaptic vesicles have been commonly attributed to the very effective action of glutamate transporters present on neuronal and glial cells. This view however does not take into account the fact that the brain is highly vascularized and that the vasculature harbors a high density of glutamate transporters. In this article, we review the accumulated data establishing the existence of an efflux of excess Glu from brain extracellular fluids into blood. We describe plausible mechanisms accounting for this efflux and present evidence that the brain-to-blood Glu efflux is modulated by blood Glu levels and can be accelerated by blood Glu scavenging. The latter procedure shown here to afford brain neuroprotection in a rat model of closed head injury could be applicable, as a first-line therapy, in the various acute brain insults characterized by excess Glu in brain fluids.

    Original languageEnglish
    Pages (from-to)301-308
    Number of pages8
    JournalNeuroscience
    Volume158
    Issue number1
    DOIs
    StatePublished - 12 Jan 2009

    Keywords

    • capillary endothelial cells
    • closed head injury
    • dual-probe microdialysis
    • glutamate transporters
    • neuroprotection

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