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Changes in astrocytic glutamate catabolism enzymes following neuronal degeneration or viral infection
Author(s) -
Belin MarieFrancoise,
DidierBazes Marianne,
Akaoka Hidéo,
HardinPouzet Hélène,
Bernard Arlette,
Giraudon Pascale
Publication year - 1997
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199709)21:1<154::aid-glia17>3.0.co;2-r
Subject(s) - biology , glutamate receptor , glutamine synthetase , catabolism , astrocyte , central nervous system , glutamate dehydrogenase , neuroscience , glutaminase , context (archaeology) , neuroglia , glutamine , homeostasis , enzyme , microbiology and biotechnology , biochemistry , amino acid , paleontology , receptor
Abstract Functional changes in astrocytes are among the earliest cellular responses to a wide variety of insults to the central nervous system (CNS). Such responses significantly contribute to maintaining CNS homeostasis. In this context, by controlling energetic metabolism and overall excitability of the CNS, the modulation of glutamate uptake and catabolism in astrocytes is crucial. Here, we review specific modulations of the expression of glutamate cabolizing enzymes (glutamate dehydrogenase and glutamine synthetase) in response to CNS insults (degeneration of serotonergic neurons or viral infection by a human retrovirus, HTLV‐I). The cellular and molecular mechanisms involved in the control of the glutamate catabolism are discussed in relation to neurological disorders. GLIA 21:154–161, 1997. © 1997 Wiley‐Liss, Inc.