中文摘要：

目的：探讨预运动训练对大鼠脑梗死后缺血侧纹状体处谷氨酸（Glu）水平及其代谢型受体（mGluR1）mRNA表达的影响,探讨预运动训练对缺血性脑梗死的保护机制。方法：将Sprague-Dawley大鼠随机分为假手术组、缺血组和缺血前运动组。运动方案采用电动跑台,30mim/d,20m/min,5d/week,共2周。采用微透析技术收集各组大鼠缺血前、缺血期间（40,80和120min）和再灌注后（40,80,120,160,200和240min）的脑细胞外液,用于测定兴奋性氨基酸Glu含量的变化。同时运用RT-PCR技术半定量分析缺血80min和再灌注240min时纹状体脑组织内的mGluR1 mRNA表达水平。结果：缺血组Glu水平在缺血40、80、120min和再灌注40、120、160min时间点与缺血前比较有显著性差异（P〈0.05,P〈0.01）。运动组各时间点的Glu水平普遍显著低于缺血组（P〈0.05,P〈0.01）,而缺血时各时间点显著高于假手术组（P〈0.05,P〈0.01）。缺血80min和再灌注240min时缺血组和运动组mGluR1 mRNA表达均显著高于假手术组,运动组显著低于缺血组（P〈0.05）。结论：预运动训练对随后发生的脑梗死纹状体内重要的兴奋性氨基酸递质Glu的过度释放有一定程度的抑制作用,这种抑制作用可能与mGluR1 mRNA的下调有某种联系。

英文摘要：

Objective To study the effect of treadmill preconditioning on the glutamate （Glu） and metabotropic glutamate receptor （mGluRs） of striatum in rats following middle cerebral artery occlusion. Methods SD rats were randomly divided into 3 groups： sham group, ischemic group and preconditioning ischemic group. The rats underwent treadmill training at the speed of 20m/min, 30min per day, 5 days per week, for total of 2 weeks. After treadmill training, middle cerebral artery was occluded for 120 minutes, followed by reperfusion. Dialysate was collected from the striatum in vivo immediately before ischemia （0 min）, and 40, 80, 120 minutes after occlusion, as well as 40, 80, 120, 160, 200 and 240 minutes after reperfusion. Brain mGluR1 mRNA expression in the striatum was detected 80 minutes after occlusion and 240 minutes after reperfusion. Results The Glu level in ischemic group 40, 80, 120min after occlusion and 40,120,160min after reperfusion was significantly different, as compare with that before occlusion （P〈0.05, P〈0.01）. The Glu level in preconditioning ischemic group was significantly lower than that in ischemic group （P〈0.05, P〈0.01）, while significantly higher than that in sham group （P〈0.05, P〈0.01）. Brain mGluR1 mRNA expression 80min after occlusion and 240min after reperfusion in ischemic group and preconditioning ischemic group was significantly higher than that in sham group （P〈0.05）, but it was significantly lower in preconditioning ischemic group than in ischemic group （P〈0.05）. Conclusion Physically preconditioning could inhibit the excessive release of Glu following cerebral ischemia, which could be related to the down regulation of mGluR1 mRNA.