Department of Medicine and Program in Neurosciences, Faculty of Sciences and Fribourg Center for Cognition, University of Fribourg, Chemin du Musée 5, CH-1700 Fribourg, Switzerland.
Neuroscience. 2012 Dec 27;227:271-82. doi: 10.1016/j.neuroscience.2012.09.052. Epub 2012 Oct 2.
In adult macaque monkeys subjected to an incomplete spinal cord injury (SCI), corticospinal (CS) fibers are rarely observed to grow in the lesion territory. This situation is little affected by the application of an anti-Nogo-A antibody which otherwise fosters the growth of CS fibers rostrally and caudally to the lesion. However, when using the Sternberger monoclonal-incorporated antibody 32 (SMI-32), a marker detecting a non-phosphorylated neurofilament epitope, numerous SMI-32-positive (+) fibers were observed in the spinal lesion territory of 18 adult macaque monkeys; eight of these animals had received a control antibody infusion intrathecally for 1 month after the injury, five animals an anti-Nogo-A antibody, and five animals received an anti-Nogo-A antibody together with brain-derived neurotrophic factor (BDNF). These fibers occupied the whole dorso-ventral axis of the lesion site with a tendency to accumulate on the ventral side, and their trajectories were erratic. Most of these fibers (about 87%) were larger than 1.3 μm and densely SMI-32 (+) stained. In the undamaged spinal tissue, motoneurons form the only large population of SMI-32 (+) neurons which are densely stained and have large diameter axons. These data therefore suggest that a sizeable proportion of the fibers seen in the lesion territory originate from motoneurons, although fibers of other origins could also contribute. Neither the presence of the antibody neutralizing Nogo-A alone, nor the presence of the antibody neutralizing Nogo-A combined with BDNF influenced the number or the length of the SMI-32 (+) fibers in the spinal lesion area. In summary, our data show that after a spinal cord lesion in adult monkeys, the lesion site is colonized by fibers, a large portion of which presumably originate from motoneurons.
在不完全性脊髓损伤（SCI）的成年猕猴中，很少观察到皮质脊髓（CS）纤维在损伤部位生长。这种情况很少受到抗 Nogo-A 抗体的影响，抗 Nogo-A 抗体否则会促进 CS 纤维在损伤的上下方向生长。然而，当使用 Sternberger 单克隆抗体 32（SMI-32）时，一种检测非磷酸化神经丝表位的标记物，在 18 只成年猕猴的脊髓损伤部位观察到大量的 SMI-32 阳性（+）纤维；其中 8 只动物在损伤后 1 个月鞘内给予对照抗体，5 只动物给予抗 Nogo-A 抗体，5 只动物给予抗 Nogo-A 抗体和脑源性神经营养因子（BDNF）。这些纤维占据了损伤部位的整个背腹轴，倾向于聚集在腹侧，其轨迹不稳定。这些纤维中的大多数（约 87%）大于 1.3 μm，且密集染色为 SMI-32（+）。在未受损的脊髓组织中，运动神经元形成唯一的大型 SMI-32（+）神经元群体，这些神经元染色密集，轴突粗大。因此，这些数据表明，在损伤部位观察到的纤维中有相当大的一部分来源于运动神经元，尽管其他来源的纤维也可能存在。单独中和 Nogo-A 的抗体的存在，或中和 Nogo-A 结合 BDNF 的抗体的存在，都不会影响脊髓损伤区域中 SMI-32（+）纤维的数量或长度。总之，我们的数据表明，在成年猕猴的脊髓损伤后，损伤部位被纤维占据，其中很大一部分可能来源于运动神经元。
