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Lactate contributes to ammonia-mediated astroglial dysfunction during hyperammonemia.

Anna Andersson ; Louise Adermark ; Mikael Persson ; Anna Westerlund ; Torsten Olsson (Institutionen för signaler och system, Medicinska signaler och system) ; Elisabeth Hansson
Neurochemical research (1573-6903). Vol. 34 (2009), 3, p. 556-65.
[Artikel, refereegranskad vetenskaplig]

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.

Nyckelord: 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

Denna post skapades 2009-12-18. Senast ändrad 2014-12-09.
CPL Pubid: 104239


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Institutioner (Chalmers)

Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering (2006-2016)
Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi (GU)
Institutionen för signaler och system, Medicinska signaler och system (2005-2017)



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