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Increased extracellular brain glutamate in acute liver failure: Decreased uptake or increased release?

Item Type:Article
Title:Increased extracellular brain glutamate in acute liver failure: Decreased uptake or increased release?
Creators Name:Rose, C.
Abstract:Glutamatergic dysfunction has been suggested to play an important role in the pathogenesis of hepatic encephalopathy (HE) in acute liver failure (ALF). Increased extracellular brain glutamate concentrations have consistently been described in different experimental animal models of ALF and in patients with increased intracranial pressure due to ALF. High brain ammonia levels remain the leading candidate in the pathogenesis of HE in ALF and studies have demonstrated a correlation between ammonia and increased concentrations of extracellular brain glutamate both clinically and in experimental animal models of ALF. Inhibition of glutamate uptake or increased glutamate release from neurons and/or astrocytes could cause an increase in extracellular glutamate. This review analyses the effect of ammonia on glutamate release from (and uptake into) both neurons and astrocytes and how these pathophysiological mechanisms may be involved in the pathogenesis of HE in ALF.
Keywords:Acute Liver Failure, Ammonia, Astrocytes, Glutamate, Hepatic Encephalopathy, Animals
Source:Metabolic Brain Disease
ISSN:0885-7490
Publisher:Kluwer Academic/Plenium Publ (U.S.A.)
Volume:17
Number:4
Page Range:251-261
Date:December 2002
Official Publication:https://doi.org/10.1023/A:1021945515514
PubMed:View item in PubMed

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