Glutamate metabolism is down-regulated in astrocytes during experimental allergic encephalomyelitis

H Hardin-Pouzet, M Krakowski, L Bourbonnière, M Didier-Bazes, E Tran, T Owens

Research output: Contribution to journalJournal articleResearchpeer-review


Experimental allergic encephalomyelitis (EAE) was induced in SJL/J mice by adoptive transfer of MBP-reactive T cells in order to investigate the role of astrocytes in pathology. GFAP protein and mRNA expression (analyzed using semiquantitative Western blot and RT-PCR techniques) were upregulated in the spinal cord of mice, which had developed a complete paralysis of hind- and fore-limbs and tail (grade 4 EAE), thus establishing that reactive gliosis occurred under these experimental conditions. Within the same samples and using similar techniques, we found that glutamine synthetase (GS) and glutamate dehydrogenase (GDH) expression were dramatically reduced. These two astrocytic enzymes are responsible for degradation of glutamate, the most abundant excitatory neurotransmitter in the brain. Since elevated levels of glutamate may be neurotoxic, we propose that the decreased capacity of astrocytes to metabolize glutamate may contribute to EAE pathology.
Original languageEnglish
Issue number1
Pages (from-to)79-85
Number of pages6
Publication statusPublished - 1. May 1997


  • Adoptive Transfer
  • Animals
  • Astrocytes
  • Brain
  • Encephalomyelitis, Autoimmune, Experimental
  • Female
  • Glial Fibrillary Acidic Protein
  • Glutamate Dehydrogenase
  • Glutamate-Ammonia Ligase
  • Glutamic Acid
  • Mice
  • Mice, Inbred Strains
  • Myelin Basic Proteins
  • Paralysis
  • Polymerase Chain Reaction
  • RNA, Messenger
  • Spinal Cord
  • T-Lymphocytes
  • Transcription, Genetic

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