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目的 本文旨在研究局灶性脑缺血时 ,大鼠脑内NMDA受体的活性变化。方法 线拴法阻塞大鼠大脑中动脉制成局灶性脑缺血模型。以 [3H]TCP为配基 ,采用放射自显影观察NMDA受体的活性变化。结果 缺血 1h、 2h和 4h组缺血侧纹状体、皮层损伤区 [3H]TCP结合位点密度显著高于非缺血侧 (P <0 0 5 ) ,缺血 1h即达峰值 (P <0 0 1)。三组 [3H]TCP结合位点密度增高区域面积均明显大于梗死区面积 (I1、I2P <0 0 1;I4P <0 0 5 )。结论 局灶性脑缺血可引发NMDA受体活性迅速持续升高。梗死区周围的半暗带内 ,NMDA受体处于持续激活状态。
Objective This study aimed to investigate the changes of NMDA receptor activity in the rat brain during focal cerebral ischemia. Methods Tethered middle cerebral artery occlusion rat model made of focal cerebral ischemia. Using [3H] TCP as ligand, the changes of NMDA receptor activity were observed by autoradiography. Results The density of [3H] TCP binding sites in ischemic cortex and cortex in ischemic 1h, 2h and 4h groups were significantly higher than those in the non-ischemic (P <0 05) and peaked at 1h <0 0 1). The area of [3H] TCP binding site density increased in three groups were significantly larger than the infarct size (I1, I2P <0 0 1; I4P <0 05). Conclusion Focal cerebral ischemia can lead to rapid and sustained increase of NMDA receptor activity. NMDA receptors are continuously activated in the penumbra around the infarct zone.