Rubinov Mikail, McIntosh Anthony R, Valenzuela Michael J, Breakspear Michael
School of Psychiatry, University of New South Wales, Sydney, NSW, Australia.
Am J Geriatr Psychiatry. 2009 Mar;17(3):210-7. doi: 10.1097/JGP.0b013e318187137a.
The authors utilize a model of activity-dependent neuronal plasticity to study the interplay between synaptogenesis, neuronal death, and neurogenesis on the resulting pattern of neuronal connectivity.
A mathematical model of neuronal network activity was employed, with plasticity instantiated by an activity-dependent rewiring rule. In particular, the authors modeled a neural system as a collection of "nodes" (neural subsystems) connected by "links" (anatomical connectivity). Neuronal damage was simulated by deletion of nodes in this evolving network through either random or targeted attack. Neurogenesis was likewise simulated by insertion of new nodes with random connections.
Local and global structural network properties were characterized using the metrics of local and global "efficiency," and network "reachability."
Activity-dependent plasticity yields a network that is robust to random node deletion, with preservation of a "small-world" architecture, characterized by high local and global efficiency. In contrast, targeted deletion of central nodes leads to a drop in reachability and global efficiency, with a consequent loss of small-world properties. Simulated neurogenesis is able to compensate for this targeted cell loss even when rates of new cell formation are considerably slower than that of simulated cell death.
The rapid growth of computational neuroscience enables to study the interplay between neuronal plasticity and cell death in computational models of brain network activity. Although the current simulations lack much of the rich physiology of real neuronal systems, they nevertheless allow us to make tentative hypotheses of the effects of neuronal lesions on the resulting neuroanatomical connectivity networks.
作者利用一种依赖活动的神经元可塑性模型,研究突触形成、神经元死亡和神经发生之间的相互作用对最终神经元连接模式的影响。
采用了一个神经元网络活动的数学模型,通过依赖活动的重新布线规则来实例化可塑性。具体而言,作者将神经系统建模为通过“链接”(解剖学连接)连接的“节点”(神经子系统)集合。通过随机或定向攻击删除这个不断演化的网络中的节点来模拟神经元损伤。同样,通过插入具有随机连接的新节点来模拟神经发生。
使用局部和全局“效率”以及网络“可达性”指标来表征局部和全局结构网络特性。
依赖活动的可塑性产生一个对随机节点删除具有鲁棒性的网络,保留了以高局部和全局效率为特征的“小世界”架构。相比之下,中央节点的定向删除会导致可达性和全局效率下降,从而失去小世界特性。即使新细胞形成速率远低于模拟细胞死亡速率,模拟的神经发生也能够补偿这种定向细胞损失。
计算神经科学的快速发展使得能够在脑网络活动的计算模型中研究神经元可塑性和细胞死亡之间的相互作用。尽管当前的模拟缺乏真实神经元系统丰富的生理学特征,但它们仍然使我们能够对神经元损伤对由此产生的神经解剖连接网络的影响做出初步假设。