Chew Cory, Sengelaub Dale R
Psychological and Brain Sciences, Indiana University, Bloomington, IN, USA.
Neural Regen Res. 2020 Aug;15(8):1373-1376. doi: 10.4103/1673-5374.274323.
Injuries to spinal motoneurons manifest in a variety of forms, including damage to peripheral axons, neurodegenerative disease, or direct insult centrally. Such injuries produce a variety of negative structural and functional changes in both the directly affected and neighboring motoneurons. Exercise is a relatively simple behavioral intervention that has been demonstrated to protect against, and accelerate recovery from, these negative changes. In this article, we describe how exercise is neuroprotective for motoneurons, accelerating axon regeneration following axotomy and attenuating dendritic atrophy following the death of neighboring motoneurons. In both of these injury models, the positive effects of exercise have been found to be dependent on gonadal hormone action. Here we describe a model in which exercise, hormones, and brain-derived neurotrophic factor might all interact to produce neuroprotective effects on motoneuron structure following neural injury.
脊髓运动神经元损伤表现为多种形式，包括外周轴突损伤、神经退行性疾病或中枢直接损伤。此类损伤会在直接受影响的运动神经元以及相邻运动神经元中产生各种负面的结构和功能变化。运动是一种相对简单的行为干预方式，已被证明可预防这些负面变化并加速从中恢复。在本文中，我们描述了运动如何对运动神经元具有神经保护作用，加速轴突切断后的轴突再生，并减轻相邻运动神经元死亡后的树突萎缩。在这两种损伤模型中，均发现运动的积极作用依赖于性腺激素的作用。在此我们描述一种模型，其中运动、激素和脑源性神经营养因子可能相互作用，对神经损伤后的运动神经元结构产生神经保护作用。
