The neurotransmitter glutamate is involved in fast excitatory synaptic transmission in the mammalian brain. Glutamate released from presynaptic terminals must be removed rapidly from the synaptic cleft by high affinity, sodium-dependent glutamate transporters to keep the extracellular glutamate concentration low to protect neuron from glutamate excitotoxicity, which is the major pathological mechanism of brain ischemia. GLAST is one of the identified four subtypes of the glutamate 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 expression and cerebral ischemia. Nonradioactive in situ hybridization was employed to evaluate the changes of glutamate transporter GLAST mRNA expression in rat cerebral cortex and hippocampus following photochemically induced focal cortical ischemia. GLAST mRNA expression in cerebral pyramid cells below the infarcted area did not change at 3 h, significantly decreased at 12 h, recovered to the control level at 24 h, and significantly increased at 72 h following the ischemic lesion. No changes in GLAST mRNA expression were observed in all subfields of the hippocampal complex. The present findings suggest that the time-course changes of GLAST mRNA expression after ischemia may be correlated with the pathogenesis of photosensitive ischemic brain damage.