Ikemoto A, Hirano A
Department of Pathology, Montefiore Medical Center, Bronx, New York, NY 10467, USA.
Acta Neuropathol. 1996 Nov;92(5):473-8. doi: 10.1007/s004010050549.
This report concerns a comparative study of alterations of anterior horn presynaptic terminals in post-poliomyelitis and sporadic amyotrophic lateral sclerosis (S-ALS). Synaptophysin (SP) served as a marker for presynaptic terminals; immunohistochemical techniques were used throughout. Spinal cords from six individuals without neurological disease served as controls. Localized and well-delineated anterior horn neuropil areas with decreased SP immunoreactivity were observed in the five cases of post-poliomyelitis studied. These areas had few remaining neurons but had pronounced reactive gliosis which corresponded to those areas in which typical poliomyelitis lesions were present. Normal neuronal SP expression was preserved in the adjacent, non-affected areas. However, a small region with increased SP levels was observed in one case. By comparison, the decrease in anterior horn SP immunoreactivity was diffuse in the four S-ALS patients studied. The present data suggest that presynaptic terminals ending at the somata and processes of affected anterior horn neurons located in the area of the acute infection are degenerate in post-poliomyelitis. By contrast, in S-ALS the terminals ending at distal dendrite portions tend to be severely degenerate, while those terminating at the proximal portions of the neuron are relatively well preserved. Our results thus provide additional evidence that the pathogenesis of the post-poliomyelitis state differs from that of ALS.
本报告涉及小儿麻痹后遗症和散发性肌萎缩侧索硬化症(S-ALS)前角突触前终末改变的比较研究。突触素(SP)用作突触前终末的标志物;全程采用免疫组织化学技术。来自6名无神经疾病个体的脊髓用作对照。在所研究的5例小儿麻痹后遗症病例中,观察到前角神经毡区域局部且界限清晰,SP免疫反应性降低。这些区域剩余神经元很少,但有明显的反应性胶质增生,与存在典型小儿麻痹症病变的区域相对应。相邻未受影响区域的神经元SP表达正常。然而,在1例病例中观察到一个SP水平升高的小区域。相比之下,在所研究的4例S-ALS患者中,前角SP免疫反应性的降低是弥漫性的。目前的数据表明,在小儿麻痹后遗症中,终止于急性感染区域受影响前角神经元胞体和突起的突触前终末发生退化。相比之下,在S-ALS中,终止于远端树突部分的终末往往严重退化,而终止于神经元近端部分的终末相对保存完好。因此,我们的结果提供了额外的证据,表明小儿麻痹后遗症状态的发病机制与ALS不同。