[Liver failure and neurotransmitters of central nervous system]

Abstract

There is increasing evidence that alternations of glutamatergic function are implicated in the pathogenesis of central nervous system consequences of hyperammonemia in liver failure. Concentrations of ammonium ion are increased and it leads to uncontrolled production of glutamine from these ions, so it is responsible for damage of the brain. Increasing concentrations of glutamine in the brain have a direct effect on glutamatergic neurotransmission, because number of binding sites for glutamatergic receptors changes. A number of binding sites for glutamatergic receptors: non-NMDA, AMPA and kainate is decreased in hippocampus, cerebral cortex, hypothalamus and cerebellum, while the binding sites for the NMDA receptor were within normal limits. Diminished expression of glutamatergic receptors leads to hypofunction of these receptors. So we can say about correlation between hyperammonemia in liver failure to distribution and activity of glutamine and glutamate as a neurotransmitter of CNS.