Spatial organisation of the mesoscale connectome: A feature influencing synchrony and metastability of network dynamics.
Spatial organisation of the mesoscale connectome: A feature influencing synchrony and metastability of network dynamics.
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DOI：
10.1371/journal.pcbi.1011349
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发表时间：
2023-08
影响因子：
4.3
通讯作者：
中科院分区：
文献类型：
--
作者：
重要的研究调查了大脑网络的同步，但这项工作的大部分是探索了大脑网络在宏观尺度上的贡献。在这里，我们探讨了改变网络拓扑对代表中尺度新皮质的空间受限随机网络中功能动力学的影响。我们使用 Kuramoto 模型来模拟网络动力学，并探索系统的同步和临界动力学作为随机生成的网络中拓扑的函数，具有与距离相关的布线概率并且没有优先连接项。我们展示了主要使短距离连接平滑关键耦合点并表现出更大的亚稳态的网络，从而产生更广泛的耦合强度，展示了临界动力学和亚稳态。我们展示了这些几何约束网络中集群同步的出现，功能组织沿着结构连接发生，从而最小化集群的参与系数。我们表明，这些内部同步节点组也表现为弱耦合节点，并显示与集群间交互相关的集群内去同步和重新同步事件。虽然簇同步似乎对健康的大脑功能至关重要，但如果它导致牢不可破的局部同步（这种情况可能发生在极端拓扑中），那么它也可能是病态的，这对癫痫研究、更广泛的大脑功能和社交网络等其他领域都有影响。大量研究调查了大脑网络如何导致癫痫等疾病。迄今为止，这项工作的大部分内容都在探索宏观尺度的连通性。整个大脑区域之间。在这里，我们探讨皮层柱之间的中尺度网络的拓扑结构如何影响功能行为。我们使用简单振荡器模型； Kuramoto 模型，使用各种网络来研究网络拓扑如何影响这些振荡器彼此同步的方式。据假设，健康的大脑在一个关键点上运行，其中区域可以轻松地相互同步和去同步，这取决于节点之间的连接强度。我们表明，拓扑结构极大地影响了这种行为，并且某些模式允许这种关键行为在更广泛的连接强度上存在，从而使系统更加稳健。我们展示了振荡器在簇中同步，它们本身的行为就好像它们是单独的振荡器一样，并显示了与其他簇的相互作用。虽然这种行为对于健康的大脑功能可能是必要的，但在极端拓扑下，如果它导致牢不可破的簇同步，这可能会变得病态，并对癫痫研究和社交网络等其他领域产生影响。
Significant research has investigated synchronisation in brain networks, but the bulk of this work has explored the contribution of brain networks at the macroscale. Here we explore the effects of changing network topology on functional dynamics in spatially constrained random networks representing mesoscale neocortex. We use the Kuramoto model to simulate network dynamics and explore synchronisation and critical dynamics of the system as a function of topology in randomly generated networks with a distance-related wiring probability and no preferential attachment term. We show networks which predominantly make short-distance connections smooth out the critical coupling point and show much greater metastability, resulting in a wider range of coupling strengths demonstrating critical dynamics and metastability. We show the emergence of cluster synchronisation in these geometrically-constrained networks with functional organisation occurring along structural connections that minimise the participation coefficient of the cluster. We show that these cohorts of internally synchronised nodes also behave en masse as weakly coupled nodes and show intra-cluster desynchronisation and resynchronisation events related to inter-cluster interaction. While cluster synchronisation appears crucial to healthy brain function, it may also be pathological if it leads to unbreakable local synchronisation which may happen at extreme topologies, with implications for epilepsy research, wider brain function and other domains such as social networks. Significant research has investigated how the brain network, leads to diseases such as epilepsy. To date, most of this work has explored connectivity on the macroscale; between whole brain regions. Here we explore how the topology of mesoscale networks, between cortical columns, could affect functional behaviour. We use a model of a simple oscillator; the Kuramoto model, with a variety of networks to investigate how the network topology affects how these oscillators synchronise with each other. It is hypothesised that healthy brain operates at a critical point where regions can both synchronise and desynchronise with each other easily which is dependent on the strength of connections between nodes. We show that the topology dramatically affects this behaviour and that certain patterns allow this critical behaviour to exist over a wider range of connection strengths, making the system more robust. We show the oscillators synchronise in clusters, which themselves behave as if they were individual oscillators, and show interactions with other clusters. While this behaviour may be necessary for healthy brain function, at extreme topologies this may become pathological if it leads to unbreakable cluster synchronisation with implications for epilepsy research and other domains such as social networks.
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影响因子：
5.7
作者：
Alderson TH;Bokde ALW;Kelso JAS;Maguire L;Coyle D;Alzheimer's Disease Neuroimaging Initiative
通讯作者：
Alzheimer's Disease Neuroimaging Initiative
DOI：
10.1098/rstb.2011.0351
发表时间：
2012-04-05
期刊：
Philosophical transactions of the Royal Society of London. Series B, Biological sciences
影响因子：
--
作者：
Kelso JA
通讯作者：
Kelso JA
影响因子：
3
作者：
Hesse J;Gross T
通讯作者：
Gross T
影响因子：
4.8
作者：
Honey, Christopher J.;Sporns, Olaf
通讯作者：
Sporns, Olaf
影响因子：
3.8
作者：
Anyaeji, Chinedu, I;Cabral, Joana;Silbersweig, David
通讯作者：
Silbersweig, David