Alexianu M E, Manole E, Engelhardt J I, Appel S H
Department of Neurology, Baylor College of Medicine Houston, TX 77030, USA.
J Neurosci Res. 2000 Apr 1;60(1):98-105. doi: 10.1002/(SICI)1097-4547(20000401)60:1<98::AID-JNR10>3.0.CO;2-B.
Experimental studies have suggested that increased calcium and inappropriate calcium handling by motoneurons might have a significant role in motoneuron degeneration. To further define the involvement of calcium in motoneuron loss we used the oxalate-pyroantimonate technique for calcium fixation and monitored the ultrastructural distribution of calcium in spinal motoneurons in experimental autoimmune gray matter disease (EAGMD). In cervical and hypoglossal motoneurons from animals with relatively preserved upper extremity and bulbar function, increased calcium precipitates were present in the cytoplasm as well as in mitochondria, endoplasmic reticulum and Golgi complex without significant morphologic alterations. In surviving lumbar motoneurons of animals with hindlimb paralysis, however, there was massive morphological destruction of intracellular organelles but no significant accumulation of calcium precipitates. These findings suggest that altered calcium homeostasis is involved in motoneuron immune-mediated injury with increased calcium precipitates early in the disease process and decreased to absent calcium precipitates later in the pathogenesis of motoneuron injury.
实验研究表明，运动神经元钙含量增加及钙处理不当可能在运动神经元变性中起重要作用。为进一步明确钙在运动神经元丢失中的作用，我们采用草酸盐 - 焦锑酸盐技术进行钙固定，并监测实验性自身免疫性灰质疾病（EAGMD）中脊髓运动神经元钙的超微结构分布。在具有相对保留的上肢和延髓功能的动物的颈运动神经元和舌下运动神经元中，细胞质以及线粒体、内质网和高尔基体复合物中存在增加的钙沉淀，且无明显形态学改变。然而，在患有后肢麻痹的动物存活的腰运动神经元中，细胞内细胞器存在大量形态学破坏，但钙沉淀无明显积累。这些发现表明，钙稳态改变参与了运动神经元免疫介导的损伤，在疾病早期钙沉淀增加，而在运动神经元损伤发病机制的后期钙沉淀减少至消失。
