脑暂时性缺血后海马神经元损伤及超微结构中 Ca^(++)分布的变化

MORPHOLOGY AND ULTRASTRUCTURAL CALCIUM DISTRIBUTION OF NEURONS IN THE RAT HIPPOCAMPUS FOLLOWING TRANSIENT ISCHEMIA

阻断4条血管诱发大鼠暂时性脑缺血后,海马结构内神经元呈损伤性改变。光镜下见3种不同类型神经元损伤,以 CA1区锥体细胞的迟发性神经元死亡变化最显著;超微结构见受损锥体细胞主要累及线粒体和内质网;超微结构组织化学显示受损的线粒体及有髓神经纤维的轴索鞘内含有不等量的钙沉积。电镜观察表明,肿胀的线粒体、轴突终末及扩张的内质网即为光镜下所见的微空泡,从而证实神经元微空泡变为不可逆损伤,Ca^(++)超载进一步导致细胞死亡。对细胞内钙增加在发病机制中的重要作用进行了分析和讨论。

In the present study we examined the ischemic neuronal damage of hippocampus following transient ischemia in the rat model of four-vessel occlusion.By LM three different type of heteroge- nous changes were observed as previous paper described.Ultrastructural examination revealed the pyramidal cell with neuronal somata swollen and axon terminals dilated and edematous.The ER cisterane were distended and fragmented.In addition we used a modification of the oxalate-pyroan- timonate technigue to demonstrate the specific subeellular compartmentalization of Ca^(++)pyroanti- monate precipitates.EM examination indicated swollen mitochondria in the soma of pyramidal neu- ron and in the myelinated fibers contained different degree of calcium.The microvacuoles were in- dentified as swollen mitochondria,swollen axon terminal and dilated ER cisterane by EM.Owing to the Ca^(++)pyroantimonate precipitate found in the microvacuolation neurons it should be consid- ered as an irreverisible change and suggested Ca^(++)overload playing a critical role in the pathologi- cal process.