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dc.contributor.authorMorland, Cecilie
dc.contributor.authorPettersen, Mi Nguyen
dc.contributor.authorHassel, Bjørnar
dc.date.accessioned2017-02-14T13:33:26Z
dc.date.accessioned2017-02-22T09:20:19Z
dc.date.available2017-02-14T13:33:26Z
dc.date.available2017-02-22T09:20:19Z
dc.date.issued2016
dc.identifier.citationMorland C, Pettersen, Hassel B. 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;54:34-43en_GB
dc.identifier.urihttp://hdl.handle.net/20.500.12242/603
dc.identifier.urihttps://ffi-publikasjoner.archive.knowledgearc.net/handle/20.500.12242/603
dc.descriptionMorland, 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. 34-43en_GB
dc.description.abstractElevation 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.en_GB
dc.language.isoenen_GB
dc.subjectTermSet Emneord::Forgiftning
dc.subjectTermSet Emneord::Salt
dc.titleHyperosmolar 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 calciumen_GB
dc.typeArticleen_GB
dc.date.updated2017-02-14T13:33:26Z
dc.identifier.cristinID1361710
dc.identifier.cristinID1361710
dc.identifier.doi10.1016/j.neuro.2016.03.005
dc.source.issn0161-813X
dc.source.issn1872-9711
dc.type.documentJournal article


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