Homeostatic structural plasticity can account for topology changes following deafferentation and focal stroke
Homeostatic structural plasticity can account for topology changes following deafferentation and focal stroke
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DOI：
10.3389/fnana.2014.00115
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发表时间：
2014-10-16
影响因子：
2.9
通讯作者：
van Ooyen, Arjen
中科院分区：
文献类型：
--
作者：
Butz, Markus;Steenbuck, Ines D.;van Ooyen, Arjen
在肿瘤或中风引起的脑损伤后，或在持续的输入丧失（传入神经阻滞）后，区域间和区域内的脑网络会以复杂的拓扑变化做出反应。不仅直接受病变影响的区域，而且远离病变的区域也可能改变它们的连通性，这种现象称为神经联系不能。脑损伤后网络拓扑结构的变化可导致认知能力下降和功能障碍增加。然而，对网络拓扑变化的原理知之甚少。在这里，我们调查了稳态结构可塑性是否可以解释传入神经阻滞和脑损伤后网络拓扑结构的变化。稳态结构可塑性假设神经元旨在通过在神经元活动太高时删除突触以及在活动太低时提供新的突触接触来维持期望水平的电活动。使用我们的结构可塑性模型，我们探讨了局部变化的连接引起的焦点损失的输入影响全球网络拓扑结构。根据实验和临床数据，我们发现，在部分去传入后，网络作为一个整体变得更加随机，虽然它保持其小世界拓扑结构，而去传入神经元增加了它们的介数中心性，因为它们重新连接并返回到稳态活动范围。此外，去传入神经元增加了它们的整体效率，但降低了它们的局部效率，并得到了较长的尾部度分布，表明中枢神经元的出现。总之，我们的研究结果表明，稳态结构可塑性可能是病变诱导的网络重组的重要驱动力，并且去传入区域介数中心性的增加可能是脑修复的生物标志物。
After brain lesions caused by tumors or stroke, or after lasting loss of input (deafferentation), inter- and intra-regional brain networks respond with complex changes in topology. Not only areas directly affected by the lesion but also regions remote from the lesion may alter their connectivity a phenomenon known as diaschisis. Changes in network topology after brain lesions can lead to cognitive decline and increasing functional disability. However, the principles governing changes in network topology are poorly understood. Here, we investigated whether homeostatic structural plasticity can account for changes in network topology after deafferentation and brain lesions. Homeostatic structural plasticity postulates that neurons aim to maintain a desired level of electrical activity by deleting synapses when neuronal activity is too high and by providing new synaptic contacts when activity is too low. Using our Model of Structural Plasticity, we explored how local changes in connectivity induced by a focal loss of input affected global network topology. In accordance with experimental and clinical data, we found that after partial deafferentation, the network as a whole became more random, although it maintained its small-world topology, while deafferentated neurons increased their betweenness centrality as they rewired and returned to the homeostatic range of activity. Furthermore, deafferentated neurons increased their global but decreased their local efficiency and got longer tailed degree distributions, indicating the emergence of hub neurons. Together, our results suggest that homeostatic structural plasticity may be an important driving force for lesion-induced network reorganization and that the increase in betweenness centrality of deafferentated areas may hold as a biomarker for brain repair.