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Neurochem Int. 2002 Aug-Sep;41(2-3):81-5.

Glutamate transporters in hyperammonemia.

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Neuroscience Research Unit, Hôpital Saint-Luc du Chum, University of Montreal, 1058 St-Denis Street, Que., H2X 3J4, Montreal, Canada.


Evidence suggests that increases in brain ammonia due to congenital urea cycle disorders, Reye Syndrome or liver failure have deleterious effects on the glutamate neurotransmitter system. In particular, ammonia exposure of the brain in vivo or in vitro preparations leads to alterations of glutamate transport. Exposure of cultured astrocytes to ammonia results in reduced high affinity uptake sites for glutamate due to a reduction in expression of the astrocytic glutamate transporter GLAST. On the other hand, acute liver failure leads to decreased expression of a second astrocytic glutamate transporter GLT-1 and a consequent reduction in glutamate transport sites in brain. Effects of the chronic exposure of brain to ammonia on cellular glutamate transport are less clear. The loss of glutamate transporter activity in brain in acute liver failure and hyperammonemia is associated with increased extracellular brain glutamate concentrations which may be responsible for the hyperexcitability and cerebral edema observed in hyperammonemic disorders.

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