Abstract:
:Glial glutamate transporter-1 (GLT-1) is the predominant subtype of glutamate transporters which are responsible for the homeostasis of extracellular glutamate. Our previous studies have shown that up-regulation in GLT-1 protein expression matches brain ischemic tolerance induced by cerebral ischemic preconditioning (CIP). To specify the role of functional changes of GLT-1 in the induction of brain ischemic tolerance by CIP, the present study was undertaken to examine changes in the binding properties of GLT-1 (including maximum binding and affinity for glutamate) and in GLT-1 mediated glutamate uptake, using L-³H-glutamate assay in the rat hippocampus. The results indicated that CIP was able to increase the maximum binding and affinity, and uptake of GLT-1 for glutamate in hippocampal CA1 subfield either with or without the presence of the subsequent severe brain ischemic insult. Simultaneously, accompanied with the above changes, CIP significantly reduced the delayed neuronal death (DND) in this region induced by lethal global cerebral ischemia. It could be concluded that up-regulation in the maximum binding and affinity and glutamate uptake of GLT-1 contributed to the neuronal protection of CIP against global cerebral ischemic insult.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Liu AJ,Hu YY,Li WB,Xu J,Zhang Mdoi
10.1111/j.1471-4159.2011.07396.xsubject
Has Abstractpub_date
2011-10-01 00:00:00pages
202-9issue
1eissn
0022-3042issn
1471-4159journal_volume
119pub_type
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