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Publication Detail
Bilirubin does not modulate ionotropic glutamate receptors or glutamate transporters
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Warr O, Mort D, Attwell D
  • Publication date:
    2000
  • Pagination:
    13, 16
  • Journal:
    Brain Research
  • Volume:
    879
  • Issue:
    1
  • Print ISSN:
    0006-8993
  • Keywords:
    Alzheimer's disease, AMPA receptors, bilirubin, Blood, Brain, Carbon Monoxide, cell, CELLS, disease, glial cells, glutamate, jaundice, metabolism, neonatal, neuron, neurons, physiology, pyramidal cell, Receptor, synthesis, transporters, uptake
  • Addresses:
    Department of Physiology, University College London, Gower Street, WC1E 6BT, London, UK
Abstract
Bilirubin, a product of haemoglobin metabolism, has been suggested to damage neurons by increasing activation of N-methyl-D-aspartate (NMDA) receptors when it reaches high levels in the blood [15,19], as occurs in neonatal jaundice [7]. Bilirubin is also generated in the brain following synthesis of the messenger carbon monoxide (CO) by haem oxygenase, and haem oxygenase is upregulated in Alzheimer's disease [23]. We examined the effect of bilirubin on currents generated by NMDA and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors in hippocampal pyramidal cells, and on glutamate transporter currents in retinal glial cells. Bilirubin did not modulate either receptor-gated currents or transporter currents. These data show the negative, but important result that bilirubin does not induce neuronal death by acting directly on NMDA or AMPA receptors, nor indirectly by blocking glutamate uptake and raising the extracellular concentration of glutamate
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