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- W936769156 abstract "The central role of hyperammonemia in hepatic encephalopathy is now well recognized. In recent years, a number of excellent reviews have appeared on the metabolic effects of ammonia (Benjamin,1982; Kvamme,1983a; Cooper and Plum,1987). The purpose of this review is to examine one possible link between the metabolic and neurological effects of ammonia, namely the inhibition of glutaminase by ammonia. Glutaminase, mostly located in nerve terminals (Bradford and Ward, 1976), converts glutamine to glutamate and ammonia. There is extensive evidence to show that glutamine is synthesized in astroglia (Martinez-Hernandez et al., 1977) and then taken up by terminals where it is the major source of transmitter glutamate (Hamberger et al., 1979a; Szerb and O’Regan, 1985). Therefore, ammonia, by inhibiting glutaminase, can decrease the synthesis and release of the excitatory transmitter glutamate. The resulting impaired excitatory transmission could explain symptoms of CNS depression seen in hepatic encephalopathy." @default.
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- W936769156 date "1989-01-01" @default.
- W936769156 modified "2023-09-22" @default.
- W936769156 title "Does Ammonia Exert Its Neurotoxicity Through an Inhibition of Transmitter Glutamate Synthesis?" @default.
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- W936769156 doi "https://doi.org/10.1007/978-1-4612-4506-3_31" @default.
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