Document Detail

Characterization of modes of release of amino acids in the ischemic/reperfused rat cerebral cortex.
MedLine Citation:
PMID:  12742092     Owner:  NLM     Status:  MEDLINE    
Brain extracellular levels of glutamate, aspartate, GABA and glycine increase rapidly following the onset of ischemia, remain at an elevated level during the ischemia, and then decline over 20-30 min following reperfusion. The elevated levels of the excitotoxic amino acids, glutamate and aspartate, are thought to contribute to ischemia-evoked neuronal injury and death. Calcium-evoked exocytotic release appears to account for the initial (1-2 min) efflux of neurotransmitter-type amino acids following the onset of ischemia, with non-vesicular release responsible for much of the subsequent efflux of these and other amino acids, including taurine and phosphoethanolamine. Extracellular Ca(2+)-independent release is mediated, in part by Na(+)-dependent amino acid transporters in the plasma membrane operating in a reversed mode, and by the opening of swelling-induced chloride channels, which allow the passage of amino acids down their concentration gradients. Experiments on cultured neurons and astrocytes have suggested that it is the astrocytes which make the primary contribution to this amino acid efflux. Inhibition of phospholipase A(2) attenuates ischemia-evoked release of both amino and free fatty acids from the rat cerebral cortex indicating that this group of enzymes is involved in amino acid efflux, and also accounting for the consistent ischemia-evoked release of phosphoethanolamine. It is, therefore, possible that disruption of membrane integrity by phospholipases plays a role in amino acid release. Recovery of amino acid levels to preischemic levels requires their uptake by high affinity Na(+)-dependent transporters, operating in their normal mode, following restoration of energy metabolism, cell resting potentials and ionic gradients.
J W Phillis; M H O'Regan
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Neurochemistry international     Volume:  43     ISSN:  0197-0186     ISO Abbreviation:  Neurochem. Int.     Publication Date:    2003 Sep-Oct
Date Detail:
Created Date:  2003-05-13     Completed Date:  2003-08-19     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  8006959     Medline TA:  Neurochem Int     Country:  England    
Other Details:
Languages:  eng     Pagination:  461-7     Citation Subset:  IM    
Department of Physiology, Wayne State University School of Medicine, 540 E. Canfield, Detroit, MI 48201, USA.
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MeSH Terms
Amino Acids / metabolism*
Cerebral Cortex / metabolism*
Reperfusion Injury / metabolism*
Reg. No./Substance:
0/Amino Acids

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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