Terro F, Yardin C, Esclaire F, Ayer-Lelievre C, Hugon J
Histology and Cell Biology Department, Faculty of Medicine, Limoges, France.
Brain Res. 1998 Nov 2;809(2):319-24. doi: 10.1016/s0006-8993(98)00883-x.
Motoneuron death could be produced by higher sensitivity to excitoxicity during the development and pathological conditions. We report here that in ventral spinal cord cultures mild kainate exposure (12.5 microM, 20 min or 100 microM, 2.5 min) induced selective cobalt stain of motoneurons, indicating a specific Ca2+ entry through the Ca(2+)-permeable AMPA/kainate receptors. This result was associated with a selective motoneuron death as previously described. In these cultures, motoneuron immunoreactivity for the Ca2+ buffering protein, calretinin was negative. These findings suggest that the selective motoneuron death due to a mild excitotoxic insult could be linked to a marked Ca2+ influx associated with the lack of some Ca2+ buffering proteins.
在发育过程和病理条件下，运动神经元死亡可能是由于对兴奋毒性的更高敏感性所致。我们在此报告，在腹侧脊髓培养物中，轻度的海藻酸盐暴露（12.5微摩尔，20分钟或100微摩尔，2.5分钟）诱导了运动神经元的选择性钴染色，表明通过Ca（2+）渗透性AMPA/海藻酸盐受体有特定的Ca2+内流。该结果与先前描述的选择性运动神经元死亡相关。在这些培养物中，运动神经元对Ca2+缓冲蛋白钙视网膜蛋白的免疫反应性为阴性。这些发现表明，由于轻度兴奋毒性损伤导致的选择性运动神经元死亡可能与缺乏某些Ca2+缓冲蛋白相关的明显Ca2+内流有关。
