Havton L A, Kellerth J O
Department of Neurology and Brain Research Institute, Neurologic Rehabilitation and Neural Repair Programs, University of California, Los Angeles, CA. 90095-1769, USA.
J Neurocytol. 2001 Nov;30(11):917-26. doi: 10.1023/a:1020669201697.
An incomplete motor nerve injury or a partial loss of motoneurons leads to a partial denervation of skeletal muscle. As part of a compensatory response, the remaining intact motoneurons undergo peripheral sprouting and increase their motor unit size. Our knowledge about the responses in the more proximal parts of these sprouting motoneurons is sparse, however. We investigated the effects of an incomplete transection of the medial gastrocnemius (MG) nerve in the adult cat on the morphology of the intramedullary axon and axon collateral systems of the remaining intact MG motoneurons. At twelve weeks following the partial transection of the MG nerve, intracellular recording and labeling techniques were used to deposit horseradish peroxidase into single intact MG motoneurons for detailed morphological studies. The light microscopic appearance and caliber of the intramedullary stem motor axons of the intact MG motoneurons were indistinguishable from controls. The number and size of the intramedullary motoraxon collateral systems were also unchanged. However, frequent and marked hypertrophy of the distal portions of the motoraxon collaterals was encountered. Electron microscopic studies of the hypertrophied collaterals demonstrated abnormal accumulations of disorganized neurofilaments arranged in bundles or whorls. The morphological changes were indistinguishable from the neurofilamentous hypertrophy that has previously been reported in Wallerian degeneration, in experimental and human motor neuron disease and in some regenerating axonal processes of spinal motoneurons. We conclude that, neurofilamentous hypertrophy of the intramedullary arbors of motor axons may also be part of a reactive and non-degenerative response in intact motoneurons undergoing compensatory peripheral sprouting.
不完全性运动神经损伤或运动神经元部分丧失会导致骨骼肌部分失神经支配。作为一种代偿反应的一部分,剩余完整的运动神经元会发生外周芽生并增大其运动单位大小。然而,我们对这些芽生运动神经元更近端部分的反应了解甚少。我们研究了成年猫内侧腓肠肌(MG)神经不完全横断对剩余完整MG运动神经元的髓内轴突和轴突侧支系统形态的影响。在MG神经部分横断后12周,采用细胞内记录和标记技术将辣根过氧化物酶注入单个完整的MG运动神经元,以进行详细的形态学研究。完整MG运动神经元的髓内主干运动轴突的光学显微镜外观和直径与对照组无明显差异。髓内运动轴突侧支系统的数量和大小也未改变。然而,我们发现运动轴突侧支的远端频繁且明显肥大。对肥大侧支的电子显微镜研究显示,有排列成束状或漩涡状的杂乱神经丝异常聚集。这些形态学变化与先前在沃勒变性、实验性和人类运动神经元疾病以及脊髓运动神经元的一些再生轴突过程中报道的神经丝肥大无法区分。我们得出结论,运动轴突髓内分支的神经丝肥大也可能是完整运动神经元在进行代偿性外周芽生时的一种反应性和非退行性反应的一部分。