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  • Andersson, AnnaGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation,University of Gothenburg (author)

Lactate contributes to ammonia-mediated astroglial dysfunction during hyperammonemia.

  • Article/chapterEnglish2009

Publisher, publication year, extent ...

  • 2008-08-21
  • Springer Science and Business Media LLC,2009

Numbers

  • LIBRIS-ID:oai:gup.ub.gu.se/104239
  • https://gup.ub.gu.se/publication/104239URI
  • https://doi.org/10.1007/s11064-008-9819-1DOI
  • https://research.chalmers.se/publication/104239URI

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  • Language:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • 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.

Subject headings and genre

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  • Adermark, Louise,1974Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,University of Gothenburg(Swepub:gu)xadelo (author)
  • Persson, Mikael,1979Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation,University of Gothenburg(Swepub:gu)xpmike (author)
  • Westerlund, Anna,1981Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation,University of Gothenburg(Swepub:gu)xwesta (author)
  • Olsson, Torsten,1937Chalmers tekniska högskola,Chalmers University of Technology(Swepub:cth)torsten (author)
  • Hansson, Elisabeth,1955Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation,University of Gothenburg(Swepub:gu)xhanse (author)
  • Göteborgs universitetInstitutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering (creator_code:org_t)

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  • In:Neurochemical research: Springer Science and Business Media LLC34:3, s. 556-651573-69030364-3190

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