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

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Udgivelsesdato: 1997-May
OriginalsprogEngelsk
TidsskriftGlia
Vol/bind20
Udgave nummer1
Sider (fra-til)79-85
Antal sider6
ISSN0894-1491
StatusUdgivet - 1. maj 1997

Fingeraftryk

Autoimmune Experimental Encephalomyelitis
Glutamic Acid
Pathology
Glutamate Dehydrogenase
Glutamate-Ammonia Ligase
Gliosis
Neurotransmitter Agents
Polymerase Chain Reaction
Messenger RNA
Enzymes
Proteins

Citer dette

Hardin-Pouzet, H., Krakowski, M., Bourbonnière, L., Didier-Bazes, M., Tran, E., & Owens, T. (1997). Glutamate metabolism is down-regulated in astrocytes during experimental allergic encephalomyelitis. Glia, 20(1), 79-85.
Hardin-Pouzet, H ; Krakowski, M ; Bourbonnière, L ; Didier-Bazes, M ; Tran, E ; Owens, T. / Glutamate metabolism is down-regulated in astrocytes during experimental allergic encephalomyelitis. I: Glia. 1997 ; Bind 20, Nr. 1. s. 79-85.
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title = "Glutamate metabolism is down-regulated in astrocytes during experimental allergic encephalomyelitis",
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 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.",
keywords = "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",
author = "H Hardin-Pouzet and M Krakowski and L Bourbonni{\`e}re and M Didier-Bazes and E Tran and T Owens",
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Hardin-Pouzet, H, Krakowski, M, Bourbonnière, L, Didier-Bazes, M, Tran, E & Owens, T 1997, 'Glutamate metabolism is down-regulated in astrocytes during experimental allergic encephalomyelitis', Glia, bind 20, nr. 1, s. 79-85.

Glutamate metabolism is down-regulated in astrocytes during experimental allergic encephalomyelitis. / Hardin-Pouzet, H; Krakowski, M; Bourbonnière, L; Didier-Bazes, M; Tran, E; Owens, T.

I: Glia, Bind 20, Nr. 1, 01.05.1997, s. 79-85.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Glutamate metabolism is down-regulated in astrocytes during experimental allergic encephalomyelitis

AU - Hardin-Pouzet, H

AU - Krakowski, M

AU - Bourbonnière, L

AU - Didier-Bazes, M

AU - Tran, E

AU - Owens, T

PY - 1997/5/1

Y1 - 1997/5/1

N2 - 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.

AB - 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.

KW - Adoptive Transfer

KW - Animals

KW - Astrocytes

KW - Brain

KW - Encephalomyelitis, Autoimmune, Experimental

KW - Female

KW - Glial Fibrillary Acidic Protein

KW - Glutamate Dehydrogenase

KW - Glutamate-Ammonia Ligase

KW - Glutamic Acid

KW - Mice

KW - Mice, Inbred Strains

KW - Myelin Basic Proteins

KW - Paralysis

KW - Polymerase Chain Reaction

KW - RNA, Messenger

KW - Spinal Cord

KW - T-Lymphocytes

KW - Transcription, Genetic

M3 - Journal article

C2 - 9145307

VL - 20

SP - 79

EP - 85

JO - Glia

JF - Glia

SN - 0894-1491

IS - 1

ER -

Hardin-Pouzet H, Krakowski M, Bourbonnière L, Didier-Bazes M, Tran E, Owens T. Glutamate metabolism is down-regulated in astrocytes during experimental allergic encephalomyelitis. Glia. 1997 maj 1;20(1):79-85.