1 Indiana University, Bloomington, IN, USA.
Neurorehabil Neural Repair. 2019 Aug;33(8):656-667. doi: 10.1177/1545968319860485. Epub 2019 Jul 9.
. Motoneuron loss is a severe medical problem that can result in loss of motor control and eventually death. We have previously demonstrated that partial motoneuron loss can result in dendritic atrophy and functional deficits in nearby surviving motoneurons, and that treatment with androgens can be neuroprotective against this dendritic atrophy. Exercise has also been shown to be protective following a variety of neural injury models and, in some cases, is dependent on androgen action. . In this study, we explored whether exercise shows the same neuroprotective effect on induced dendritic atrophy as that seen with androgen treatment. . Motoneurons innervating the vastus medialis muscles of adult male rats were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Following saporin injections, some animals were allowed free access to a running wheel attached to their home cages. Four weeks later, motoneurons innervating the ipsilateral vastus lateralis muscle were labeled with cholera toxin-conjugated horseradish peroxidase, and dendritic arbors were reconstructed in 3 dimensions. . Dendritic arbor lengths of animals allowed to exercise were significantly longer than those not allowed to exercise. . These findings indicate that exercise following neural injury exerts a protective effect on motoneuron dendrites comparable to that seen with exogenous androgen treatment.
运动神经元丢失是一个严重的医学问题,可能导致运动控制丧失,并最终导致死亡。我们之前已经证明,部分运动神经元丢失会导致树突萎缩,并导致附近存活的运动神经元出现功能缺陷,而雄激素治疗可以对此种树突萎缩起到神经保护作用。运动已被证明在多种神经损伤模型中具有保护作用,在某些情况下,它依赖于雄激素的作用。在这项研究中,我们探讨了运动是否对诱导的树突萎缩表现出与雄激素治疗相同的神经保护作用。成年雄性大鼠股直肌的运动神经元被肌肉内注射霍乱毒素结合的蓖麻毒素选择性杀死。在注射蓖麻毒素后,一些动物可以自由进入连接到其笼舍的跑步轮。四周后,用霍乱毒素结合的辣根过氧化物酶标记支配对侧股外侧肌的运动神经元,并在三维空间中重建树突分支。允许运动的动物的树突分支长度明显长于不允许运动的动物。这些发现表明,神经损伤后进行运动对运动神经元树突具有与外源性雄激素治疗相当的保护作用。