Lactate Contributes to Ammonia-Mediated Astroglial Dysfunction During Hyperammonemia
Autor: | Anna K. Andersson, Torsten Olsson, Elisabeth Hansson, Mikael Persson, Louise Adermark, Anna Westerlund |
---|---|
Rok vydání: | 2008 |
Předmět: |
inorganic chemicals
Nervous system medicine.medical_specialty Biology Microfilament Biochemistry Ammonium Chloride Rats Sprague-Dawley Cellular and Molecular Neuroscience chemistry.chemical_compound Biosynthesis Ammonia Internal medicine medicine Animals Hyperammonemia Lactic Acid Cells Cultured Cell Size Neurons Microglia General Medicine Metabolism medicine.disease Coculture Techniques Rats Excitatory Amino Acid Transporter 1 Actin Cytoskeleton medicine.anatomical_structure Endocrinology Excitatory Amino Acid Transporter 2 chemistry Astrocytes Calcium Ammonium chloride Astrocyte |
Zdroj: | Neurochemical Research. 34:556-565 |
ISSN: | 1573-6903 0364-3190 |
DOI: | 10.1007/s11064-008-9819-1 |
Popis: | 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. |
Databáze: | OpenAIRE |
Externí odkaz: |