Köksal-Ersöz Elif, Benquet Pascal, Wendling Fabrice
Univ Rennes, INSERM, LTSI UMR 1099, Rennes, France.
PLoS Comput Biol. 2024 Dec 3;20(12):e1012666. doi: 10.1371/journal.pcbi.1012666. eCollection 2024 Dec.
Neuroplasticity refers to functional and structural changes in brain regions in response to healthy and pathological activity. Activity dependent plasticity induced by epileptic activity can involve healthy brain regions into the epileptogenic network by perturbing their excitation/inhibition balance. In this article, we present a new neural mass model, which accounts for neuroplasticity, for investigating the possible mechanisms underlying the epileptogenic network expansion. Our multiple-timescale model is inspired by physiological calcium-mediated synaptic plasticity and pathological extrasynaptic N-methyl-D-aspartate (NMDA) dependent plasticity dynamics. The model highlights that synaptic plasticity at excitatory connections and structural changes in the inhibitory system can transform a healthy region into a secondary epileptic focus under recurrent seizures and interictal activity occurring in the primary focus. Our results suggest that the latent period of this transformation can provide a window of opportunity to prevent the expansion of epileptogenic networks, formation of an epileptic focus, or other comorbidities associated with epileptic activity.
神经可塑性是指大脑区域因健康和病理活动而发生的功能和结构变化。由癫痫活动诱导的活动依赖性可塑性可通过扰乱其兴奋/抑制平衡，将健康脑区纳入致痫网络。在本文中，我们提出了一种新的神经团块模型，该模型考虑了神经可塑性，用于研究致痫网络扩展的潜在机制。我们的多时间尺度模型受生理钙介导的突触可塑性和病理突触外N-甲基-D-天冬氨酸（NMDA）依赖性可塑性动力学的启发。该模型强调，在原发性病灶发生反复癫痫发作和发作间期活动时，兴奋性连接的突触可塑性和抑制系统的结构变化可将健康区域转变为继发性癫痫病灶。我们的结果表明，这种转变的潜伏期可为预防致痫网络扩展、癫痫病灶形成或与癫痫活动相关的其他合并症提供一个机会窗口。
