Sasaki S, Iwata M
Department of Neurology, Tokyo Women's Medical College, Japan.
Acta Neuropathol. 1996;91(4):416-21. doi: 10.1007/s004010050444.
This report concerns an ultrastructural investigation of the synapses of anterior horn neurons in the lumbar spinal cord of four patients with lower motor neuron disease (LMND) who had no upper motor neuron and corticospinal tract involvement. Anterior horn neurons of five normal individuals served as controls. The cell body area and the number of synapses of the normal-appearing neurons of the LMND patients were significantly reduced (P < 0.0001). These findings suggest that synaptic changes of anterior horn neurons could be ascribed to the degeneration of lower motor neurons rather than to the influence of upper motor neuron system degeneration. On the other hand, the lengths of individual synapses (P < 0.0001) and of their active zones (P < 0.05) were significantly increased in the patients. These increases would indicate that synapses on anterior horn neurons of individuals with LMND appear to have the capacity to react to progressive degeneration and loss of other synapses by means of a compensatory response or plasticity that enhances their efficiency.
本报告涉及对4例无上位运动神经元和皮质脊髓束受累的下运动神经元疾病（LMND）患者腰脊髓前角神经元突触的超微结构研究。选取5例正常个体的前角神经元作为对照。LMND患者中外观正常的神经元的细胞体面积和突触数量显著减少（P < 0.0001）。这些发现表明，前角神经元的突触变化可归因于下运动神经元的退化，而非上位运动神经元系统退化的影响。另一方面，患者个体突触的长度（P < 0.0001）及其活性区的长度（P < 0.05）显著增加。这些增加表明，患有LMND的个体前角神经元上的突触似乎有能力通过增强其效率的代偿反应或可塑性来应对其他突触的进行性退化和丧失。
