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

H Hardin‐Pouzet, M Krakowski, L Bourbonniére… - Glia, 1997 - Wiley Online Library
H Hardin‐Pouzet, M Krakowski, L Bourbonniére, M Didier‐Bazes, E Tran, T Owens
Glia, 1997Wiley Online Library
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 semi‐quantitative 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 …
Abstract
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 semi‐quantitative 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. GLIA 20:79–85, 1997. © 1997 Wiley‐Liss, Inc.
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