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作 者:张忱[1] 孟书聪[2] 徐亚萍[1] 程兰英[1]
机构地区:[1]中日友好临床医学研究所,100029 [2]北京医科大学细胞生物室
出 处:《中华神经外科杂志》2001年第5期321-323,共3页Chinese Journal of Neurosurgery
基 金:国家九五医学攻关项目 ( 96 90 6 0 2 0 1)
摘 要: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 To study the alteration of NMDA receptor activity during focal cerebral ischemia injury in rats. Methods The focal cerebral ischemia rat model was made by occluding the middle cerebral artery(MCA) with thread. An autoradiographic study in vivo was used to observe the activity of NMDA receptor with TCP as the binding ligand. Results The density of TCP binding sites were greater in the territory of the occluded MCA, most prominently in the caudate nucleus and cortex, than that in the equivalent areas in the contralaterl hemisphere in 1 hour, 2 hour and 4 hours after ischemia (P<0 05). The levels of isotope culminated following 1h of focal cerebral ischemia (P<0 01). The brain region where the binding density rised was much larger than the infarction size in I1,I2 and I4 (I1,I2 P<0 01; I4<0 05). Conclusions Focal cerebral ischemia can result in prompt and continuous increase of NMDA receptor activity. NMDA receptors would be excited continuously in the penumbra around the ischemia core.
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