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 an androgen‐dependent effect of exercise following injury can be neuroprotective against this dendritic atrophy. In this study, we explored where the necessary site of androgen action is for exercise‐driven neuroprotective effects on induced dendritic atrophy. Motoneurons innervating the vastus medialis muscles of adult male rats were selectively killed by intramuscular injection of cholera toxin‐conjugated saporin. Simultaneously, some saporin‐injected animals were given implants of the androgen receptor antagonist hydroxyflutamide, either directly at the adjacent vastus lateralis musculature ipsilateral to the saporin‐injected vastus medialis or interscapularly as a systemic control. Following saporin injections, some animals were allowed free access to a running wheel attached to their home cages. Four weeks later, motoneurons innervating the same vastus lateralis muscle were labeled with cholera toxin‐conjugated horseradish peroxidase, and dendritic arbors were reconstructed in three dimensions. Dendritic arbor lengths of saporin‐injected animals allowed to exercise were significantly longer than those not allowed to exercise. Androgen receptor blockade locally at the vastus lateralis muscle prevented the protective effect of exercise. These findings indicate that exercise following neural injury exerts a protective effect on motoneuron dendrites, which acts via androgen receptor action at the target muscle.

中文翻译：

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在邻近运动神经元死亡后，运动对目标肌肉的雄激素作用对体细胞运动神经元的形态具有神经保护作用

运动神经元丢失是一个严重的医学问题，可导致运动控制丧失并最终死亡。我们之前已经证明，部分运动神经元缺失会导致附近存活的运动神经元的树突萎缩和功能缺陷，并且损伤后运动的雄激素依赖性作用可以对这种树突萎缩具有神经保护作用。在这项研究中，我们探讨了雄激素作用的必要部位是运动驱动的神经保护作用对诱导的树突萎缩的影响。通过肌肉注射霍乱毒素结合皂草素选择性地杀死支配成年雄性大鼠股内侧肌的运动神经元。同时，一些注射皂草素的动物被植入了雄激素受体拮抗剂羟基氟他胺，直接在邻近的股外侧肌组织与注射皂素的股内侧肌同侧或肩胛间作为全身控制。注射皂草素后，一些动物被允许自由使用附在它们家笼子上的跑轮。4 周后，支配同一股外侧肌的运动神经元被标记为霍乱毒素偶联辣根过氧化物酶，并在三个维度上重建了树突状乔木。允许运动的注射皂草素的动物的树突乔木长度明显长于不允许运动的动物。股外侧肌局部的雄激素受体阻断阻止了运动的保护作用。这些发现表明，神经损伤后的运动对运动神经元树突具有保护作用，