Jacob J M, Robbins N
Center for Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.
J Neurosci. 1990 May;10(5):1530-40. doi: 10.1523/JNEUROSCI.10-05-01530.1990.
The effect of age on the ability of motor neurons to develop and maintain an enlarged total axonal and synaptic volume was compared in soleus muscles of 5-8-month and 25-30-month mice, 30-120 d after partial denervation. Before and after partial denervation (transection of the L5 root), the total number of muscle fibers was the same in all muscles. However, in young animals, there was only some transient atrophy and hypertrophy mostly receded by 120 d, whereas in old muscle, a more prominent early atrophy was followed by persistent hypertrophy. Ectopic endplates were not found. In zinc-iodide-osmium (ZIO) stained preparations, muscle fibers with small nerve terminals were present at 60 d and were still present in old muscle at 120 d. Fluorescent staining of nerve terminals and acetylcholine receptors revealed that in young muscle, postsynaptic sites were nearly or completely reoccupied by 60 d. In old muscle, about 22% of former junctions were denervated, with the remainder minimally to fully reinnervated. At 60 d and thereafter, collateral sprouts originated from nodes of Ranvier in both young and old muscle and were remyelinated in young but mainly unmyelinated and remarkably tortuous in old animals. These results, confirmed with immunofluorescent strains for myelin basic protein and neurofilaments, account for many of the physiological findings (Jacob and Robbins, 1990). Motor unit size expanded 2.5 times in young and 2 times in old muscle at 60 d after partial denervation. However, the increment in total quantal output and nerve terminal volume per motor neuron was 60-100% greater than control in young but only 20-25% greater in old muscle, with little further recovery. This inability of the motor neuron in old mice to expand the field of innervation may reflect a limitation imposed by reduced axonal transport. The present findings may elucidate the muscle weakness in postpolio syndrome and amyotrophic lateral sclerosis.
在部分去神经支配后30 - 120天，比较了5 - 8月龄和25 - 30月龄小鼠比目鱼肌中年龄对运动神经元发育和维持增大的总轴突及突触体积能力的影响。在部分去神经支配（L5神经根横断）前后，所有肌肉中的肌纤维总数相同。然而，在年轻动物中，仅出现了一些短暂的萎缩和肥大，大多在120天时消退，而在老年肌肉中，早期萎缩更明显，随后是持续的肥大。未发现异位终板。在碘化锌锇（ZIO）染色的标本中，有小神经末梢的肌纤维在60天时出现，在120天时仍存在于老年肌肉中。神经末梢和乙酰胆碱受体的荧光染色显示，在年轻肌肉中，突触后位点在60天时几乎或完全重新被占据。在老年肌肉中，约22%的先前连接去神经支配，其余部分部分至完全重新神经支配。在60天及之后，侧支芽在年轻和老年肌肉中均起源于郎飞结，并在年轻动物中重新髓鞘化，但在老年动物中主要未髓鞘化且明显迂曲。这些结果通过髓鞘碱性蛋白和神经丝的免疫荧光染色得到证实，解释了许多生理学发现（雅各布和罗宾斯，1990年）。部分去神经支配后60天，年轻肌肉中运动单位大小扩大了2.5倍，老年肌肉中扩大了2倍。然而，每个运动神经元的总量子输出和神经末梢体积的增加在年轻肌肉中比对照大60 - 100%，而在老年肌肉中仅比对照大20 - 25%，几乎没有进一步恢复。老年小鼠运动神经元无法扩大神经支配范围可能反映了轴突运输减少所带来的限制。目前的发现可能阐明了小儿麻痹后遗症和肌萎缩侧索硬化症中的肌肉无力。
