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• W3144908114 abstract "Ammonia, which is considered to be the main agent responsible for hepatic encephalopathy, inhibits oxidative glucose metabolism in the brain. However, the effects of ammonia on cerebral glucose metabolism in different brain regions remains unclear. To clarify this issue, we added ammonia directly to fresh rat brain slices and measured its effects on glucose metabolism. Dynamic positron autoradiography with ( 18 F)2-fluoro-2-deoxy-D- glucose and 2-(4-iodophenyl)-3-(4-nitrophenyl)-5-(2,4-di- sulfophenyl)-2H-tetrazolium (WST-1) colorimetric assay revealed that ammonia significantly increased the cerebral glucose metabolic rate and depressed mitochondrial func- tion, as compared to the unloaded control in each of the brain regions examined (cerebral cortex, striatum, and cerebellum), reflecting increased glycolysis that compen- sates for the decrease in aerobic metabolism. Pre-treatment with (?)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclo- hepten-5,10-imine hydrogen maleate (MK-801), a N-methyl-D-aspartate (NMDA) receptor antagonist, sig- nificantly attenuated these changes induced by ammonia in cerebellum, but not in cerebral cortex or striatum. The addition of ammonia induced an increase in cyclic gua- nosine monophosphate (cGMP) levels in cerebellum, but not in cerebral cortex or striatum, reflecting the activation of the NMDA receptor-nitric oxide-cGMP pathway. These results suggested that NMDA receptor activation is responsible for the impairment of glucose metabolism induced by ammonia specifically in cerebellum." @default.
• W3144908114 created "2021-04-13" @default.
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• W3144908114 date "2013-01-01" @default.
• W3144908114 modified "2023-09-24" @default.
• W3144908114 title "Region-specific causal mechanism in the effects of ammonia on cerebral glucose metabolism in the rat brain" @default.
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