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Lactate contributes to ammonia-mediated astroglial dysfunction during hyperammonemia.

Journal article
Authors Anna Andersson
Louise Adermark
Mikael Persson
Anna Westerlund
Torsten Olsson
Elisabeth Hansson
Published in Neurochemical research
Volume 34
Issue 3
Pages 556-65
ISSN 1573-6903
Publication year 2009
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 556-65
Language en
Links dx.doi.org/10.1007/s11064-008-9819-...
Keywords Ammonia, metabolism, Ammonium Chloride, pharmacology, Animals, Astrocytes, metabolism, pathology, Calcium, metabolism, Cell Size, Cells, Cultured, Coculture Techniques, Excitatory Amino Acid Transporter 1, biosynthesis, Excitatory Amino Acid Transporter 2, biosynthesis, Hyperammonemia, metabolism, pathology, Lactic Acid, metabolism, pharmacology, Microfilaments, ultrastructure, Neurons, metabolism, pathology, Rats, Rats, Sprague-Dawley
Subject categories Toxicology, Neurobiology

Abstract

Even though ammonia is considered to underlie nervous system symptoms of dysfunction during hyperammonemia, lactate, which increases as a metabolic consequence of high ammonia levels, might also be a contributing factor. The data presented here show that NH4Cl (5 mM) mediates astroglial cell swelling, and that treatment with NH4Cl or lactate (25 mM) causes rearrangements of actin filaments and reduces astroglial glutamate uptake capacity. Co-application with BaCl2, which blocks astroglial uptake of NH4+, prevents NH4Cl-mediated cell swelling and rearrangement of actin filaments, but does not reduce NH4Cl-induced glutamate uptake capacity inhibition. Neither NH4Cl nor lactate affected glutamate uptake or protein expression in microglial cultures, indicating that astroglial cells are more susceptible to the neurotoxic affects of ammonia. Our results suggest that ammonium underlies brain edema, but that lactate can contribute to some of the cellular dysfunctions associated with elevated cerebral levels of ammonia.

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