钙激活钾通道在钙离子致神经细胞损伤中的作用  

Kinetics of the Ca2+Activated K+ Channel in Ca2+ Induced Cortex Neurons Damage

作　　者：赖晓晖[1] 朱文梅[1] 袁光固[1] 

机构地区：[1]华西医科大学附属第一医院神经内科

出　　处：《华西医科大学学报》1999年第2期151-154,共4页Journal of West China University of Medical Sciences

摘　　要：采用膜片钳单通道记录方法，观察原代培养新生ＳＤ大鼠皮层神经元的钙激活钾通道（ＫＣａ）特征及胞内不同游离钙水平对通道开放动力学的调节。结果显示：培养ＳＤ大鼠皮层神经元的ＫＣａ以大电导活动占优势，胞内游离钙为１０－８ｍｏｌ／Ｌ时，通道几乎不开放，在１０－６ｍｏｌ／Ｌ时达最大激活。由此表明神经元上ＫＣａ通道开放概率明显依赖于胞浆中钙离子和膜电位，ＫＣａ对胞内钙离子浓度变化极为敏感。钾通道的开放剂可能有一定的神经细胞保护作用。Ca2+activated K+ channels were studied by using the patch clamp technique of single channel recordings from the primary culture fetal SD rat cortex nourons. Besides their physiologic characters, the effects of increasing cytosolic and cytoplasmic Ca2+ triggered neuronal damage were also studied. The results showed that KCa with conductance around 170PS was predominant in the rat cortex neurons. These channels almost did not open at physiologic intracellular free Ca2+ concentration (10-8 mol/L),but was extremly activated at intracellular free Ca2+ concentration (10-6 mol/L). So the open probabilities of the KCa in the cortex neurons obviously dependend on the concentration of cytoplasmic Ca2+ and membrane potential. The KCa activated by increasing of intracellular Ca2+ during the early stage of anoxia may be a protective reaction of ischemic neurons.

关 键 词：钙激活钾通道 神经元 脑缺血 神经细胞损伤 

分 类 号：R743.310.5[医药卫生—神经病学与精神病学]