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

Authors: Hardin-Pouzet, H  Krakowski, M  Bourbonniere, L  Didier-Bazes, M  Tran, E  Owens, T 
Citation: Hardin-Pouzet H, etal., Glia. 1997 May;20(1):79-85.
Pubmed: (View Article at PubMed) PMID:9145307

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.


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CRRD ID: 6484657
Created: 2012-06-27
Species: All species
Last Modified: 2012-06-27
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.