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
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.