Hyperammonemia compromises glutamate metabolism and reduces BDNF in the rat hippocampus

Neurotoxicology
Fabiana GallandMarina Concli Leite

Abstract

Ammonia is putatively the major toxin associated with hepatic encephalopathy (HE), a neuropsychiatric manifestation that results in cognitive impairment, poor concentration and psychomotor alterations. The hippocampus, a brain region involved in cognitive impairment and depressive behavior, has been studied less than neocortical regions. Herein, we investigated hippocampal astrocyte parameters in a hyperammonemic model without hepatic lesion and in acute hippocampal slices exposed to ammonia. We also measured hippocampal BDNF, a neurotrophin commonly related to synaptic plasticity and cognitive deficit, and peripheral S100B protein, used as a marker for brain damage. Hyperammonemia directly impaired astrocyte function, inducing a decrease in glutamate uptake and in the activity of glutamine synthetase, in turn altering the glutamine-glutamate cycle, glutamatergic neurotransmission and ammonia detoxification itself. Hippocampal BDNF was reduced in hyperammonemic rats via a mechanism that may involve astrocyte production, since the same effect was observed in astrocyte cultures exposed to ammonia. Ammonia induced a significant increase in S100B secretion in cultured astrocytes; however, no significant changes were observed in the...Continue Reading

Citations

Jun 17, 2020·Molecular Neurobiology·Larissa Daniele BoberminAndré Quincozes-Santos
Jun 27, 2019·Scientific Reports·Alba-Aina CastellsÀngels Garcia-Cazorla
Feb 7, 2021·Liver International : Official Journal of the International Association for the Study of the Liver·Rafael Ochoa-SanchezChristopher F Rose
Jun 16, 2021·Neurochemical Research·Rafael Ochoa-SanchezChristopher F Rose
Oct 28, 2019·EBioMedicine·Kaihui LuAndreas S Reichert

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