Neuroprotective Effects on the Morphology of Somatic Motoneurons Following the Death of Neighboring Motoneurons: A Role for Microglia?
Neuroprotective Effects on the Morphology of Somatic Motoneurons Following the Death of Neighboring Motoneurons: A Role for Microglia?
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邻近运动神经元死亡后对体细胞运动神经元形态的神经保护作用：小胶质细胞的作用？
DOI：
10.1002/dneu.22652
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发表时间：
2019
影响因子：
3
通讯作者：
Sengelaub,DaleR
中科院分区：
文献类型：
--
作者：
Chew,Cory;Kiley,BrandonJ;Sengelaub,DaleR
脊髓运动神经元群体的部分耗竭诱导邻近运动神经元的树突状萎缩，并且用睾酮治疗保护运动神经元免于诱导的树突状萎缩。我们探讨了一个潜在的机制，这种诱导萎缩和保护睾酮，检查小胶质细胞的反应，部分耗尽的运动神经元。通过肌内注射霍乱毒素结合皂草素杀死支配成年雄性大鼠股内侧肌的运动神经元;一些注射皂草素的大鼠接受睾酮处理。随后通过免疫组织化学染色观察小胶质细胞，分类为监测或激活，并进行体视学计数。部分运动神经元耗竭增加了四头肌运动池中激活的小胶质细胞的数量，睾酮治疗可减弱这种增加。小胶质细胞反应的衰减可能反映了睾酮抑制小胶质细胞活化的作用，可能会保留运动神经元树突。或者，睾酮可能是神经保护性的，保留运动神经元树突，其次导致小胶质细胞活化减少。为了区分这些假设，部分运动神经元耗竭后，用米诺环素处理大鼠以抑制小胶质细胞活化。支配同侧股外侧肌的运动神经元随后用霍乱毒素结合的辣根过氧化物酶标记，并重建树突状乔木。米诺环素减少小胶质细胞活化并不能阻止部分运动神经元耗竭后诱导的树突萎缩。此外，米诺环素治疗减少小胶质细胞活化导致完整动物的树突萎缩。总之，这些研究结果表明，运动神经元死亡后，睾丸激素对树突的神经保护作用不是由于抑制小胶质细胞的激活，小胶质细胞的活性有助于正常维护树突乔木。
Partial depletion of spinal motoneuron populations induces dendritic atrophy in neighboring motoneurons, and treatment with testosterone protects motoneurons from induced dendritic atrophy. We explored a potential mechanism for this induced atrophy and protection by testosterone, examining the microglial response to partial depletion of motoneurons. Motoneurons innervating the vastus medialis muscles of adult male rats were killed by intramuscular injection of cholera toxin‐conjugated saporin; some saporin‐injected rats were treated with testosterone. Microglia were later visualized via immunohistochemical staining, classified as monitoring or activated, and counted stereologically. Partial motoneuron depletion increased the number of activated microglia in the quadriceps motor pool, and this increase was attenuated with testosterone treatment. The attenuation in microglial response could reflect an effect of testosterone on suppressing microglia activation, potentially sparing motoneuron dendrites. Alternatively, testosterone could be neuroprotective, sparing motoneuron dendrites, secondarily resulting in reduced microglial activation. To discriminate between these hypotheses, following partial motoneuron depletion, rats were treated with minocycline to inhibit microglial activation. Motoneurons innervating the ipsilateral vastus lateralis muscle were later labeled with cholera toxin‐conjugated horseradish peroxidase, and dendritic arbors were reconstructed. Reduction of microglial activation by minocycline did not prevent induced dendritic atrophy following partial motoneuron depletion. Further, reduction of microglial activation by minocycline treatment resulted in dendritic atrophy in intact animals. Together, these findings indicate that the neuroprotective effect of testosterone on dendrites following motoneuron death is not due to inhibiting microglial activation, and that microglial activity contributes to the normal maintenance of dendritic arbors.
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影响因子：
4.8
作者：
Verhovshek,Tom;Sengelaub,DaleR
通讯作者：
Sengelaub,DaleR
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影响因子：
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DOI：
--
发表时间：
2002
期刊：
The Journal of comparative neurology
影响因子：
--
作者：
S. L. Hebbeler;T. Verhovshek;D. Sengelaub
通讯作者：
D. Sengelaub
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DOI：
--
发表时间：
2009
期刊：
影响因子：
--
作者：
D. Sengelaub
通讯作者：
D. Sengelaub
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DOI：
10.1002/neu.1059
发表时间：
2001
期刊：
Journal of neurobiology.
影响因子：
--
作者：
Hebbeler,SL;Verhovshek,T;Sengelaub,DR
通讯作者：
Sengelaub,DR