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Effect of ammonia on astrocytic glutamate uptake/release mechanisms

Item Type:Article
Title:Effect of ammonia on astrocytic glutamate uptake/release mechanisms
Creators Name:Rose, C.
Abstract:Hyperammonemic disorders such as acute liver failure (ALF) or urea cycle enzymopathies are associated with hyperexcitability, seizures, brain edema and increased extracellular brain glutamate. Mechanisms responsible for increased glutamate content in the extracellular space of the brain include decreased uptake by perineuronal astrocytes and/or increased release from neurons and/or astrocytes. Exposure of astrocytes to millimolar concentrations of ammonia results in cell swelling, loss of expression of the glutamate transporters excitatory amino acid transporter (EAAT-1) and EAAT-2 and increased release of glutamate. Three distinct mechanisms are theoretically possible to explain ammonia-induced glutamate release from astrocytes namely: release due to swelling; reversal of glutamate transporters and due to Ca(2+)-dependent vesicular release. Recent identification of vesicular docking and fusion proteins in astrocytes together with glutamate-release (due to intracellular alkanization and mobilization of intracellular Ca(2+)-stores) studies implies that vesicular release is a predominant mechanism responsible for ammonia-induced release of glutamate from astrocytes.
Keywords:Acute Liver Failure, Ammonia, Astrocytes, Brain Edema, Glutamate
Source:Journal of Neurochemistry
ISSN:0022-3042
Publisher:Blackwell Publishing (U.K.)
Volume:97
Number:Suppl 1
Page Range:11-15
Date:April 2006
Official Publication:https://doi.org/10.1111/j.1471-4159.2006.03796.x
PubMed:View item in PubMed

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