ALTERED EXPRESSION OF GLUTAMATE TRANSPORTER GLAST MESSENGER-RNA IN RAT-BRAIN AFTER PHOTOCHEMICALLY INDUCED FOCAL ISCHEMIA

Authors
Citation
Kj. Yin et al., ALTERED EXPRESSION OF GLUTAMATE TRANSPORTER GLAST MESSENGER-RNA IN RAT-BRAIN AFTER PHOTOCHEMICALLY INDUCED FOCAL ISCHEMIA, The Anatomical record, 251(1), 1998, pp. 9-14
Citations number
32
Categorie Soggetti
Anatomy & Morphology
Journal title
ISSN journal
0003276X
Volume
251
Issue
1
Year of publication
1998
Pages
9 - 14
Database
ISI
SICI code
0003-276X(1998)251:1<9:AEOGTG>2.0.ZU;2-U
Abstract
Background: The neurotransmitter glutamate is involved in fast excitat ory synaptic transmission in the mammalian brain. Glutamate released f rom presynaptic terminals must be removed rapidly from the synaptic cl eft by high affinity, sodium-dependent glutamate transporters to keep the extracellular glutamate concentration low to protect neuron from g lutamate excitotoxicity, which is the major pathological mechanism of brain ischemia. GLAST is one of the identified four subtypes of the gl utamate transporter system and has been suggested to play an important role in some pathological conditions. But until recently, very little information existed the concerning relationship between GLAST express ion and cerebral ischemia. Methods: Nonradioactive in situ hybridizati on was employed to evaluate the changes of glutamate transporter GLAST mRNA expression in rat cerebral cortex and hippocampus following phot ochemically induced focal cortical ischemia. Results: GLAST mRNA expre ssion in cerebral pyramid cells below the infarcted area did not chang e at 3 h, significantly decreased at 12 h, recovered to the control le vel at 24 h, and significantly increased at 72 h following the ischemi c lesion. No changes in GLAST mRNA expression were observed in all sub fields of the hippocampal complex. Conclusions: The present findings s uggest that the time-course changes of GLAST mRNA expression after isc hemia may be correlated with the pathogenesis of photosensitive ischem ic brain damage. (C) 1998 Wiley-Liss, Inc.