Neurotoxicity of Ammonia
Copyright policy )Neurotoxicity of Ammonia
Abnormal liver function has dramatic effects on brain functions. Hyperammonemia interferes profoundly with brain metabolism, astrocyte volume regulation, and in particular mitochondrial functions. Gene expression in the brain and excitatory and inhibitory neurotransmission circuits are also affected. Experiments with a number of pertinent animal models have revealed several potential mechanisms which could underlie the pathological phenomena occurring in hepatic encephalopathy.
- University of Helsinki Finland
- Tampere University Finland
CYCLIC GMP PATHWAY, Receptors, N-Methyl-D-Aspartate, Ammonia, CULTURED RAT ASTROCYTES, Animals, Humans, CEREBELLUM IN-VIVO, Hepatic encephalopathy, Cell Size, Glutamine-glutamate cycle, CENTRAL-NERVOUS-SYSTEM, Brain, PORTAL-SYSTEMIC ENCEPHALOPATHY, Reactive Nitrogen Species, Mitochondria, MITOCHONDRIAL PERMEABILITY TRANSITION, Biomedicine, N-methyl-D-aspartate receptors, Astrocytes, Hepatic Encephalopathy, CEREBRAL CORTICAL SLICES, ACUTE LIVER-FAILURE, INDUCED HEPATIC-ENCEPHALOPATHY, METHYL-D-ASPARTATE, Reactive oxygen species, Reactive Oxygen Species
CYCLIC GMP PATHWAY, Receptors, N-Methyl-D-Aspartate, Ammonia, CULTURED RAT ASTROCYTES, Animals, Humans, CEREBELLUM IN-VIVO, Hepatic encephalopathy, Cell Size, Glutamine-glutamate cycle, CENTRAL-NERVOUS-SYSTEM, Brain, PORTAL-SYSTEMIC ENCEPHALOPATHY, Reactive Nitrogen Species, Mitochondria, MITOCHONDRIAL PERMEABILITY TRANSITION, Biomedicine, N-methyl-D-aspartate receptors, Astrocytes, Hepatic Encephalopathy, CEREBRAL CORTICAL SLICES, ACUTE LIVER-FAILURE, INDUCED HEPATIC-ENCEPHALOPATHY, METHYL-D-ASPARTATE, Reactive oxygen species, Reactive Oxygen Species
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