摘要
为探索谷氨酸受体（GluR）在介导谷氨酸（Glu）对缺血神经元损伤的作用机制，本实验建立大鼠大脑中动脉阻塞（MCAO）局部脑缺血实验模型，应用受体的放射配基结合分析（RBA）等技术动．态监测了缺血及再灌流期缺血灶、海马和下丘脑Glu、GluR含量及其亲和力的变化。结果发现：缺血30min，各脑区Glu含量达高峰，再灌流6h，Glu含量回降至基线水平，再灌流48h后，Glu含量再次中等程度升高，并持续至再灌流72h。GluR和KD值与Glu含量密切相关。结果提示，缺血再灌流早期，GluR在高浓度Glu的作用下发生同种特异性反向调节，GluR亲和力为增敏反应；再灌流中晚期，GluR的变化属于同种特异性正向调节，而GluR亲和力测为减敏反应。
In order to explore the pathophysiologic mechanism of glutamate (Glu) and glutamate reecptor (GluR) in ischemic nerural damage, using the model of middle cerebral artery occusion (MCAO). we determined the changes of Glu, GluR levels and it's KD values in hypothalamus, hipocampus and ischemic focus in rats after MCAO. Result: The Gin levies risen to peak in every determined brain areas in 30 minutes after MCAO, and reduced to base-line level in 6 hours after recitculation. Glu levels second times rise after 24 hours of recirculation, and keep to 72 hours of recirculstion- Glu, GluR levels and the KD values of GluR in same location are closed connection each other. The resalt suggested that GluR manifestated the down-reglulation to the effects of Gln and the affinity of GluR is increare in early period of ischemia and recircolation. However, GluR is up -regulation and the affinity of GluR is decrease in moderate-later period after recircalation.
出处
《脑与神经疾病杂志》
1997年第4期202-205,共4页
Journal of Brain and Nervous Diseases
关键词
谷氨酸
受体
大脑中动脉阻塞
脑缺血
Glutamate Glutamate Receptor Rat Middle cerebral Artery Occusion
