目的 研究臂丛离断后脊髓运动神经元树突退变与时间和损伤距离的相关性。 方法 在距离椎间孔3 mm或10 mm处处离断小鼠臂丛，术后7、14、28、56 d取材，采用MAP2免疫荧光染色和体视学分析、Golgi-Cox染色和Sholl分析观测颈膨大处脊髓前角运动神经元的树突结构和形态变化；术后28 d比较距离椎间孔3 mm和10 mm臂丛离断对脊髓运动神经元树突的影响。 结果 MAP2免疫荧光显示臂丛离断导致脊髓前角内树突的密度和完整性随时间延长逐渐下降；Golgi-Cox染色和Sholl分析显示运动神经元最长树突、总树突长度、树突最大跨度、树突3级分支的数量均呈时间依赖性下降。与距离椎间孔10 mm处离断组相比，3 mm处离断引起的树突长度退变更为明显。 结论 脊髓运动神经元树突在周围神经损伤后会发生退变，随时间延长其退变程度加重，随损伤部位与脊髓的距离延长树突长度退变程度减轻。
Abstract
Objective To study the correlation of time course and distance of brachial plexus transection on the dendritic degeneration of spinal motoneurons. Methods The brachial plexus of mice was transected at 3 mm or 10 mm from the intervertebral foramen, the spinal cord segments of C6~C7 was collected at 7, 14, 28 and 56 days post injury (dpi) and was subjected to perform MAP2 immunofluorescence staining, morphometric analysis, Golgi-Cox staining and Sholl analysis to assess the dendritic structure changes of spinal motoneurons. The effects of brachial plexus transection 3 mm and 10 mm from the foramina on spinal motor neuron dendrite was compared at 28 days after surgery. Results The brachial plexus transection resulted in that the density and integrity of dendrite in the spinal ventral horn decreased gradually with time. Golgi-Cox staining and Sholl analysis showed the longest dendrite, total dendritic length, the maximum span of dendrite and the number of third-grade dendrite branches of each spinal motoneuron decreased with time dependence. Compared with the transection at 10 mm from the intervertebral foramen, the length of dendritic degeneration in the 3 mm group was more severe. Conclusions The dendrite degeneration occurs and get worse in spinal motoneurons after peripheral nerve injury with time dependence, while the degree dendrite degeneration reduces with the extension of the distance between injury site and spinal cord.
关键词
树突； /
运动神经元； /
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臂丛离断； /
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脊髓
Key words
Dendrites; /
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Motoneuron; /
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Brachial plexus transection; /
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Spinal cord
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参考文献
[1] Beckers A, Moons L. Dendritic shrinkage after injury: a cellular killer or a necessity for axonal regeneration[J]? Neural Regen Res, 2019, 14(8): 1313-1316. DOI: 10.4103/1673-5374.253505.
[2] 王树森, 黄耀添, 褚晓朝, 等. 大鼠坐骨神经损伤后脊髓前角细胞及其树突的形态计量和超微结构研究[J]. 中华手外科杂志, 1996, 12(4): 245-248. DOI: 10.3760/cma.j.issn.1005-054X.1996.04.126.
[3] Blinzinger K, Kreutzberg G. Displacement of synaptic terminals from regenerating motoneurons by microglial cells[J]. Z Zellforsch Mikrosk Anat, 1968, 85(2): 145-157. DOI: 10.1007/BF00325030.
[4] Wu D, Klaw MC, Connors T, et al. Combining constitutively active rheb expression and chondroitinase promotes functional axonal regeneration after cervical spinal cord injury[J]. Mol Ther, 2017, 25(12): 2715-2726. DOI: 10.1016/j.ymthe.2017.08.011.
[5] Vaquié A, Sauvain A, Duman M, et al. Injured axons instruct schwann cells to build constricting actin spheres to accelerate axonal disintegration[J]. Cell Rep, 2019, 27(11): 3152-3166.e7. DOI: 10.1016/j.celrep.2019.05.060.
[6] Ruijs ACJ, Jaquet JB, Kalmijn S, et al. Median and ulnar nerve injuries: a meta-analysis of predictors of motor and sensory recovery after modern microsurgical nerve repair[J]. Plast Reconstr Surg, 2005, 116(2): 484-494, 495-496. DOI: 10.1097/01.prs.0000172896.86594.07.
[7] 阚世廉, 李桂石, 詹海华, 等. 大鼠周围神经移植修复后脊髓前角运动神经元变化的动态观察[J]. 中国临床解剖学杂志, 2016, 34(5): 534-539, 545. DOI: 10.13418/j.issn.1001-165x.2016.05.012.
[8] Alvarez FJ, Bullinger KL, Titus HE, et al. Permanent reorganization of Ia afferent synapses on motoneurons after peripheral nerve injuries[J]. Ann N Y Acad Sci, 2010, 1198: 231-241. DOI: 10.1111/j.1749-6632.2010.05459.x.
[9] Kim H, Heckman CJ. The tight relationship between asymmetric signaling and locational excitability in motoneuron dendrites[J]. Commun Integr Biol,2015,8(6): e1110657. DOI:10.1080/19420889. 2015. 1110657.
[10]Sholl DA. The measurable parameters of the cerebral cortex and their significance in its organization[J]. Prog Neurobiol, 1956, (2): 324-333. PMID: 13441807.
[11]Stuss DP, Boyd JD, Levin DB, et al. MeCP2 mutation results in compartment-specific reductions in dendritic branching and spine density in layer 5 motor cortical neurons of YFP-H mice[J]. PLoS One, 2012, 7(3): e31896. DOI: 10.1371/journal.pone.0031896.
[12] Wang HX, Liu NK, Zhang YP, et al. Treadmill training induced lumbar motoneuron dendritic plasticity and behavior recovery in adult rats after a thoracic contusive spinal cord injury[J]. Exp Neurol, 2015, 271: 368-378. DOI: 10.1016/j.expneurol.2015.07.004.
[13] Zhang YJ, Chen MM, Qiu ZL, et al. MiR-130a regulates neurite outgrowth and dendritic spine density by targeting MeCP2[J]. Protein Cell, 2016, 7(7): 489-500. DOI: 10.1007/s13238-016-0272-7.
[14] Nye DMR, Albertson RM, Weiner AT, et al. The receptor tyrosine kinase Ror is required for dendrite regeneration in Drosophila neurons[J]. PLoS Biol, 2020,18(3): e3000657. DOI: 10.1371/journal.pbio. 3000657.
[15] White MA, Lin ZQ, Kim E, et al. Sarm1 deletion suppresses TDP-43-linked motor neuron degeneration and cortical spine loss[J]. Acta Neuropathol Commun, 2019, 7(1): 166. DOI: 10.1186/s40478-019-0800-9.
[16] 刘蔡钺. 适度运动对周围神经损伤后脊髓突触可塑性变化的作用研究[D]. 上海: 第二军医大学, 2015.
[17] Wiberg R, Kingham PJ, Novikova LN. A morphological and molecular characterization of the spinal cord after ventral root avulsion or distal peripheral nerve axotomy injuries in Aadult rats[J]. J Neurotrauma, 2017, 34(3): 652-660. DOI: 10.1089/neu.2015.4378.
[18] Byers JS, Huguenard AL, Kuruppu D, et al. Neuroprotective effects of testosterone on motoneuron and muscle morphology following spinal cord injury[J]. J Comp Neurol, 2012, 520(12): 2683-2696. DOI: 10.1002/cne.23066.
[19] Kulkarni VA, Firestein BL. The dendritic tree and brain disorders[J]. Mol Cell Neurosci, 2012,50(1):10-20. DOI:10.1016/j.mcn.2012.03.005.
[20] Alder J, Kallman S, Palmieri A, et al. Neuropeptide orphanin FQ inhibits dendritic morphogenesis through activation of RhoA[J]. Dev Neurobiol, 2013, 73(10): 769-784. DOI: 10.1002/dneu.22101.
[21] Jiang MH, Ash RT, Baker SA, et al. Dendritic arborization and spine dynamics are abnormal in the mouse model of MECP2 duplication syndrome[J]. J Neurosci, 2013, 33(50): 19518-19533. DOI: 10.1523/JNEUROSCI.1745-13.2013.
[22] Tricaud N, Park HT. Wallerian demyelination: chronicle of a cellular cataclysm[J]. Cell Mol Life Sci, 2017, 74(22): 4049-4057. DOI: 10.1007/s00018-017-2565-2.
基金
国家自然科学基金（81870982，82071386）
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