Spinal motoneuron synaptic plasticity during the course of an animal model of multiple sclerosis
Spinal motoneuron synaptic plasticity during the course of an animal model of multiple sclerosis
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DOI：
10.1111/j.1460-9568.2006.05184.x
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发表时间：
2006-12-01
影响因子：
3.4
通讯作者：
Oliveira, A. L. R.
中科院分区：
文献类型：
--
作者：
Marques, K. B.;Santos, L. M. B.;Oliveira, A. L. R.
在实验性自身免疫性脑脊髓炎过程中，会出现运动和感觉功能的大量丧失，这在传统上被归因于脱髓鞘过程。在大鼠中，完全四肢瘫痪后的5天内临床症状消失，这表明脱髓鞘可能不是疾病快速发展的唯一原因。本研究调查了在实验性自身免疫性脑脊髓炎加重期和缓解期脊髓运动神经元突触覆盖的变化情况。用透射电子显微镜将突触末端分为C型、F型和S型。还使用了突触素、胶质纤维酸性蛋白以及小胶质细胞/巨噬细胞标志物F4/80的免疫组织化学分析，以便在突触变化和胶质反应之间建立关联。超微结构分析显示，在加重期，F型和S型突触末端都有强烈的回缩。从这个意义上说，剩余突触末端的覆盖面积和长度都大幅减少。然而，回缩的突触末端迅速恢复到贴近状态，尽管平均长度仍然较短。可能发生了一定程度的出芽现象，因为在缓解期后，F型突触末端的数量比对照组多。免疫组织化学分析显示，突触丧失的高峰与大胶质细胞和小胶质细胞反应的增强同时发生。我们的研究结果表明，在疾病过程中脊髓网络中发生的主要变化可能对临床症状的产生有重要影响，并有助于解释其快速恢复的原因。
During the course of experimental autoimmune encephalomyelitis, a massive loss of motor and sensitive function occurs, which has been classically attributed to the demyelination process. In rats, the clinical signs disappear within 5 days following complete tetraplegia, indicating that demyelination might not be the only cause for the rapid evolution of the disease. The present work investigated the occurrence of experimental autoimmune encephalomyelitis-induced changes of the synaptic covering of spinal motoneurons during exacerbation and after remission. The terminals were typed with transmission electron microscopy as C-, F- and S-type. Immunohistochemical analysis of synaptophysin, glial fibrillary acidic protein and the microglia/macrophage marker F4/80 were also used in order to draw a correlation between the synaptic changes and the glial reaction. The ultrastructural analysis showed that, during exacerbation, there was a strong retraction of both F- and S-type terminals. In this sense, both the covering as well as the length of the remaining terminals suffered great reductions. However, the retracted terminals rapidly returned to apposition, although the mean length remained shorter. A certain level of sprouting may have occurred as, after remission, the number of F-terminals was greater than in the control group. The immunohistochemical analysis showed that the peak of synaptic loss was coincident with an increased macro- and microglial reaction. Our results suggest that the major changes occurring in the spinal cord network during the time course of the disease may contribute significantly to the origin of the clinical signs as well as help to explain their rapid recovery.