Xu X M, Martin G F
Department of Cell Biology, Neurobiology and Anatomy, Ohio State University College of Medicine, Columbus.
J Neurotrauma. 1992 Summer;9(2):93-105. doi: 10.1089/neu.1992.9.93.
Rubral axons can grow around a lesion of their pathway in the thoracic spinal cord of developing opossums and a critical period exists for that plasticity. The critical period probably begins when rubral axons first grow into the thoracic cord, and it extends until approximately postnatal day 30. We previously noted that most rubrospinal neurons die after transection of their axon during the critical period, suggesting that plasticity results primarily from growth of axons not damaged by the lesion (Xu and Martin, J. Comp. Neurol. 279, 368-381, 1989). That observation led us to study the response of rubrospinal neurons to axotomy in more detail and at additional stages of development, using a prelabeling paradigm. We first injected fast blue (FB) into the caudal thoracic or rostral lumbar spinal cord in animals ranging from estimated postnatal day 9 to 50 and, about 4 days later, lesioned the rubrospinal tract several segments rostral to the injection. Approximately 30 days later, the animals were killed so that the red nucleus could be searched for labeled neurons. During the critical period for plasticity, rubrospinal neurons showed signs of degeneration 1 week after their axon was cut. When animals were killed 2-3 weeks after lesioning, there was an obvious decrease in axotomized neurons within the red nucleus, and by 4 weeks, more than 75% of them had degenerated. The marked susceptibility of rubrospinal neurons to axotomy during the critical period for plasticity is consistent with the hypothesis that developmental plasticity of the rubrospinal tract results primarily from growth of axons that were not damaged by the lesion. Our results also suggest that survival of axotomized rubrospinal neurons increases with age.
在发育中的负鼠胸段脊髓中，红核轴突能够绕过其通路的损伤部位生长，并且这种可塑性存在一个关键期。关键期可能始于红核轴突首次长入胸段脊髓之时，并持续到出生后约第30天。我们之前注意到，在关键期内，大多数红核脊髓神经元在其轴突横断后死亡，这表明可塑性主要源于未受损伤的轴突生长（Xu和Martin，《比较神经学杂志》279卷，368 - 381页，1989年）。这一观察结果促使我们使用预标记范式，在发育的更多阶段更详细地研究红核脊髓神经元对轴突切断的反应。我们首先在估计出生后第9天至50天的动物的尾侧胸段或头侧腰段脊髓中注射快蓝（FB），大约4天后，在注射部位头侧的几个节段处损伤红核脊髓束。大约30天后，处死动物以便在红核中寻找标记的神经元。在可塑性关键期内，红核脊髓神经元在其轴突切断1周后出现退化迹象。当在损伤后2 - 3周处死动物时，红核内被切断轴突的神经元明显减少，到4周时，超过75%的此类神经元已经退化。在可塑性关键期内红核脊髓神经元对轴突切断的明显易感性与红核脊髓束发育可塑性主要源于未受损伤的轴突生长这一假设一致。我们的结果还表明，被切断轴突的红核脊髓神经元的存活率随年龄增加。
