Objective    To observe the influence of adenosine receptor A2a antagonist on the glutamate transporter GLT-1 expression in the corpus striatum of rat middle cerebral artery occlusion (MCAO) models

and investigate its mechanism of ischemic neuroprotection.     Methods    Two models of male SD rats

one suffering 2 h of cerebral ischemia and the other suffering 2 h of cerebral ischemia followed by 22 h of reperfusion

were constructed. Each model was divided in a sham operation group

an ischemia control group

and an intervention group. Adenosine receptor A2a antagonist SCH-58261 was administered to the sham operation groups and the intervention groups. The expression of GLT-1 in the corpus striatum was detected by RT-PCR and Western blotting. The cerebral infarction volume and the neurological deficit condition were also observed.     Results    There was no significant difference between the neurological deficit scores of the control group and the intervention group in the cerebral ischemia (2 h) model. There was a significant difference between the neurological deficit scores of the control group (2.50±0.55) and the intervention group (1.67±0.52) in the cerebral ischemia (2 h)-reperfusion (22 h) model (

P

<

0.05). The cerebral infarction volume (23.63±3.89) of the intervention group in the cerebral ischemia (2 h) model was decreased by 16% (

P

<

0.05) as compared to that of the control group. The cerebral infarction volume (95.12±18.22) of the intervention group in the cerebral ischemia (2 h)-reperfusion (22 h) model was decreased by 33% (

P

<

0.01) as compared to that of the control group. After SCH-58261 administration

the expression of GLT-1 in the corpus striatum of rat MCAO models during the acute ischemia stage and the ischemia-reperfusion stage was increased significantly.     Conclusion    The neuroprotection of adenosine receptor A2a antagonist against cerebral ischemia is correlated with the enhancement of GLT-1 function.