Rapid loss of glutamine synthetase from astrocytes in response to hypoxia: Implications for excitotoxicity

Lee,, Lingwood, B, Bjorkman, S, Miller, S, Poronnik, P, Barnett, N, Colditz, P and Pow, D 2010, 'Rapid loss of glutamine synthetase from astrocytes in response to hypoxia: Implications for excitotoxicity', Journal o Chemical Neuroanatomy, vol. 39, no. 3, pp. 211-220.


Document type: Journal Article
Collection: Journal Articles

Title Rapid loss of glutamine synthetase from astrocytes in response to hypoxia: Implications for excitotoxicity
Author(s) Lee,
Lingwood, B
Bjorkman, S
Miller, S
Poronnik, P
Barnett, N
Colditz, P
Pow, D
Year 2010
Journal name Journal o Chemical Neuroanatomy
Volume number 39
Issue number 3
Start page 211
End page 220
Total pages 10
Publisher Elsevier BV
Abstract We have examined brains of neonatal pigs that were rendered hypoxic. Glutamine synthetase (GS). a key enzyme in the detoxification of glutamate and ammonia, was rapidly lost from astrocytes in regions susceptible to damage, including the CA1 of hippocampus and various cortical regions. Conversely, resilient areas such as the dentate gyrus exhibited little or no loss of GS. Onset of loss was rapid, patches of loss being evident by 1 h post-insult, and loss was extensive by 24 h and did not recover by 72 h. Examination of counterstained sections revealed that GS losses preceded any overt neuronal damage. Loss of GS from astrocytes would plausibly lead to a rise in intracellular glutamate, and could explain why reversal of astrocytic glutamate transport during hypoxia/ischaemia is conceptually possible.
Keyword(s) Alzheimer's astrocyte
Ammonia
Brain
Glutamate
Ischaemia
Stroke
DOI - identifier 10.1016/j.jchemneu.2009.12.002
Copyright notice © 2009 Elsevier B.V. All rights reserved.
ISSN 0891-0618
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