Sumi Takuma, Houben Akke Mats, Yamamoto Hideaki, Kato Hideyuki, Katori Yuichi, Soriano Jordi, Hirano-Iwata Ayumi
Advanced Institute for Materials Research (WPI-AIMR), Tohoku University, Sendai, Japan.
Departament de Física de la Matèria Condensada, Universitat de Barcelona, Barcelona, Spain.
Front Neurosci. 2025 Jun 19;19:1570783. doi: 10.3389/fnins.2025.1570783. eCollection 2025.
Impaired brain function is restored following injury through dynamic processes that involve synaptic plasticity. This restoration is supported by the brain's inherent modular organization, which promotes functional separation and redundancy. However, it remains unclear how modular structure interacts with synaptic plasticity to define damage response and recovery efficiency. In this work, we numerically modeled the response and recovery to damage of a neuronal network bearing a modular structure. The simulations aimed at capturing experimental observations in cultured neurons with modular traits which were physically disconnected through a focal lesion. The damage reduced the frequency of spontaneous collective activity events in the cultures, which recovered to pre-damage levels within 24 h. We rationalized this recovery in the numerical simulations by considering a plasticity mechanism based on spike-timing-dependent plasticity, a form of synaptic plasticity that modifies synaptic strength based on the relative timing of pre- and postsynaptic spikes. We observed that the numerical model effectively captured the decline and subsequent recovery of spontaneous activity following the injury. The model supports that the combination of modularity and plasticity confers robustness to the damaged neuronal network by preventing the total loss of spontaneous network-wide activity and facilitating recovery. Additionally, by using our model within the reservoir computing framework, we show that information representation in the neuronal network improves with the recovery of network-wide activity.
脑损伤后,通过涉及突触可塑性的动态过程,受损的脑功能得以恢复。这种恢复受到大脑固有模块化组织的支持,该组织促进功能分离和冗余。然而,目前尚不清楚模块化结构如何与突触可塑性相互作用,以确定损伤反应和恢复效率。在这项工作中,我们对具有模块化结构的神经元网络损伤反应和恢复进行了数值模拟。这些模拟旨在捕捉具有模块化特征的培养神经元中的实验观察结果,这些神经元通过局灶性损伤在物理上断开连接。损伤降低了培养物中自发集体活动事件的频率,该频率在24小时内恢复到损伤前水平。我们通过考虑基于尖峰时间依赖性可塑性的可塑性机制,在数值模拟中对这种恢复进行了合理化解释,尖峰时间依赖性可塑性是一种基于突触前和突触后尖峰的相对时间来改变突触强度的突触可塑性形式。我们观察到,数值模型有效地捕捉了损伤后自发活动的下降和随后的恢复。该模型支持模块化和可塑性的结合通过防止全网络自发活动的完全丧失并促进恢复,赋予受损神经元网络鲁棒性。此外,通过在储层计算框架内使用我们的模型,我们表明随着全网络活动的恢复,神经元网络中的信息表示得到改善。