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    Hyperosmolar sodium chloride is toxic to cultured neurons and causes reduction of glucose metabolism and ATP levels, an increase in glutamate uptake, and a reduction in cytosolic calcium

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    Morland2016HyperosmolarNaCl.pdf (1.327Mb)
    Date
    2016
    Author
    Morland, Cecilie
    Pettersen, Mi Nguyen
    Hassel, Bjørnar
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    Abstract
    Elevation of serum sodium, hypernatremia, which may occur during dehydration or treatment with sodium chloride, may cause brain dysfunction and damage, but toxic mechanisms are poorly understood. We found that exposure to excess NaCl, 10–100 mmol/L, for 20 h caused cell death in cultured cerebellar granule cells (neurons). Toxicity was due to Na+, since substituting excess Na+ with choline reduced cell death to control levels, whereas gluconate instead of excess Cl− did not. Prior to cell death from hyperosmolar NaCl, glucose consumption and lactate formation were reduced, and intracellular aspartate levels were elevated, consistent with reduced glycolysis or glucose uptake. Concomitantly, the level of ATP became reduced. Pyruvate, 10 mmol/L, reduced NaCl-induced cell death. The extracellular levels of glutamate, taurine, and GABA were concentration-dependently reduced by excess NaCl; high-affinity glutamate uptake increased. High extracellular [Na+] caused reduction in intracellular free [Ca2+], but a similar effect was seen with mannitol, which was not neurotoxic. We suggest that inhibition of glucose metabolism with ensuing loss of ATP is a neurotoxic mechanism of hyperosmolar sodium, whereas increased uptake of extracellular neuroactive amino acids and reduced intracellular [Ca2+] may, if they occur in vivo, contribute to the cerebral dysfunction and delirium described in hypernatremia.
    URI
    http://hdl.handle.net/20.500.12242/603
    https://ffi-publikasjoner.archive.knowledgearc.net/handle/20.500.12242/603
    DOI
    10.1016/j.neuro.2016.03.005
    Description
    Morland, Cecilie; Pettersen, Mi Nguyen; Hassel, Bjørnar. Hyperosmolar sodium chloride is toxic to cultured neurons and causes reduction of glucose metabolism and ATP levels, an increase in glutamate uptake, and a reduction in cytosolic calcium. Neurotoxicology 2016 ;Volum 54. s. 34-43
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