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本文引用的文献

1
Neuroprotective Effects on the Morphology of Somatic Motoneurons Following the Death of Neighboring Motoneurons: A Role for Microglia?神经胶质细胞在邻近运动神经元死亡后对躯体运动神经元形态的神经保护作用:一种微胶质细胞的作用?
Dev Neurobiol. 2019 Feb;79(2):131-154. doi: 10.1002/dneu.22652. Epub 2019 Jan 7.
2
Neuroprotective effects of testosterone metabolites and dependency on receptor action on the morphology of somatic motoneurons following the death of neighboring motoneurons.睾酮代谢物的神经保护作用及其对相邻运动神经元死亡后体运动神经元形态的受体作用依赖性。
Dev Neurobiol. 2017 Jun;77(6):691-707. doi: 10.1002/dneu.22445. Epub 2016 Oct 3.
3
Exercise after spinal cord injury as an agent for neuroprotection, regeneration and rehabilitation.脊髓损伤后运动作为神经保护、再生和康复的一种手段。
Brain Res. 2015 Sep 4;1619:12-21. doi: 10.1016/j.brainres.2015.03.052. Epub 2015 Apr 9.
4
VEGF-B selectively regenerates injured peripheral neurons and restores sensory and trophic functions.血管内皮生长因子-B选择性地使受损的外周神经元再生,并恢复感觉和营养功能。
Proc Natl Acad Sci U S A. 2014 Dec 2;111(48):17272-7. doi: 10.1073/pnas.1407227111. Epub 2014 Nov 17.
5
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Physiology (Bethesda). 2014 Nov;29(6):437-45. doi: 10.1152/physiol.00028.2014.
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Exercise and sex steroid hormones in skeletal muscle.骨骼肌中的运动与性类固醇激素
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7
Enhancement of peripheral nerve regeneration due to treadmill training and electrical stimulation is dependent on androgen receptor signaling.跑步机训练和电刺激所致的周围神经再生增强依赖于雄激素受体信号传导。
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Glial cell line-derived neurotrophic factor (GDNF) expression and NMJ plasticity in skeletal muscle following endurance exercise.耐力运动后胶质细胞源性神经营养因子 (GDNF) 在骨骼肌中的表达和 NMJ 可塑性。
Neuroscience. 2014 Jan 17;257:111-8. doi: 10.1016/j.neuroscience.2013.10.068. Epub 2013 Nov 8.
9
Delayed VEGF treatment enhances angiogenesis and recovery after neonatal focal rodent stroke.延迟给予血管内皮生长因子(VEGF)治疗可增强新生啮齿动物局灶性中风后的血管生成及恢复。
Transl Stroke Res. 2013 Apr;4(2):189-200. doi: 10.1007/s12975-012-0221-6.
10
Therapeutic exercise for people with amyotrophic lateral sclerosis or motor neuron disease.针对肌萎缩侧索硬化症或运动神经元病患者的治疗性运动
Cochrane Database Syst Rev. 2013 May 31;2013(5):CD005229. doi: 10.1002/14651858.CD005229.pub3.

运动对邻近运动神经元死亡后体运动神经元形态的神经保护作用。

Neuroprotective Effects of Exercise on the Morphology of Somatic Motoneurons Following the Death of Neighboring Motoneurons.

机构信息

1 Indiana University, Bloomington, IN, USA.

出版信息

Neurorehabil Neural Repair. 2019 Aug;33(8):656-667. doi: 10.1177/1545968319860485. Epub 2019 Jul 9.

DOI:10.1177/1545968319860485
PMID:31286830
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6688956/
Abstract

. 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.

摘要

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。