Document Detail

Glutamine synthetase gene expression and glutamate transporters in C6-glioma cells.
MedLine Citation:
PMID:  21107897     Owner:  NLM     Status:  In-Process    
Glutamine synthetase (GS) is the major glutamate-forming enzyme of vertebrae and is accepted to be a marker of astroglial cells. Maturation of astroglial cells is characterized by an increase in GS activity, and the regulation of this enzyme is the topic of many publications. The amino acid glutamate is the major excitatory neurotransmitter in the brain and mediates normal excitatory synaptic transmission by interaction with postsynaptic receptors. Glutamate also acts as a potent neurotoxin when present at high concentration. Glutamate neurotoxicity plays an important role in the pathophysiology of many neurological disorders, such as Alzheimer's disease, Huntington's disease and amyotrophic lateral sclerosis. In the normal condition, L-glutamate is predominantly taken up, metabolized and recycled by astrocytes through the glutamate transporters (GLAST/GLT1) and glutamine synthetase (GS) catalytic activity. Because of the fundamental role of these glutamate transporters and the glutamine synthetase enzyme in controlling cerebral glutamate level, regulation of GS and studying of the glutamate transporters in glial cells is important. Astrocytes are supportive cells and act as the site of detoxification of glutamate in the brain. However, their isolation from the brain is a tedious, costly and time consuming procedure. On the other hand, the C6-glioma cells are readily available on the market. They are well characterized and have been a useful model for CNS glia in many laboratories. For this study, we used the C6-glioma cell line as a model system. We examined the presence or absence of glial specific glutamate transporters (GLTI and GLAST) in C6-glioma cells, which was done by immunocytochemistry. We also examined glutamine synthetase gene expression in these cells by treatment of the C6-glioma cells with estrogen (17ß estradiol). The findings from this study provide useful information about C6-glioma cells which makes the study of the CNS tremendously inexpensive.
Zafeer Baber; Nasrin Haghighat
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Publication Detail:
Type:  Journal Article     Date:  2010-11-25
Journal Detail:
Title:  Metabolic brain disease     Volume:  25     ISSN:  1573-7365     ISO Abbreviation:  Metab Brain Dis     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-03     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8610370     Medline TA:  Metab Brain Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  413-8     Citation Subset:  IM    
Department of Cell Biology and Anatomy, Chicago Medical School, 3333 Green Bay Rd., North Chicago, IL 60064, USA.
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