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Yingpeng Liu

Publications and source records attributed to Yingpeng Liu.

3 recordsLinked to original sources

Role of chloride concentration in modulating seizure transitions in excitatory and inhibitory networks

Experimental evidence indicates that intracellular chloride concentration regulates the excitation and inhibition (EI) balance, yet the mechanisms by which activity-dependent chloride dynamics drive seizure evolution and stage transitions remain unclear. We present a conductance-based neuronal network in which EI balance emerges from chloride homeostasis via channel-mediated influx and transporter-mediated extrusion. We show that the fraction of inhibitory synaptic conductance contributing to channel-mediated influx acts as a control parameter that organizes seizure dynamics into distinct stages,pre-ictal, ictal-tonic, and ictal-clonic,distinguished by characteristic amplitude and frequency signatures. Decreasing this fraction shortens ictal activity and suppresses seizure initiation, whereas high fraction promotes the emergence of ictal-tonic and ictal-clonic stages and spiral-wave dynamics, rendering seizure dynamics largely insensitive to inhibition. At intermediate values, seizures bypass the ictal-tonic stage and emerge directly as the icta,clonic stage. Moreover, joint variation of fractions with synaptic strengths reveals that recurrent excitation expands the tonic-clonic seizure, while recurrent inhibition prolongs pre-ictal states and suppresses ictal-clonic activity.

q-bio.NC

Robustness and size-dependence of circadian rhythms in multiscale suprachiasmatic-nucleus networks

Understanding how multi-scale network structure influences circadian rhythms in the suprachiasmatic nucleus (SCN) is essential for uncovering the principles of rhythmic robustness and synchronization. Previous studies using synthetic SCN networks suggested a size-dependent phenomenon, in which rhythmic activity initially strengthens with network size and then saturates, but it remains unclear whether this occurs in real SCN networks. Here, we apply geometric branch growth (GBG) and geometric renormalization (GR) to generate self-similar scaled-up and scaled-down replicas from a single-scale functional mouse SCN network. Unlike synthetic models, these SCN replicas do not exhibit size-dependent rhythms: average period, amplitude, and synchronization remain stable across scales. By increasing the average degree with network size, we reproduce size-dependent rhythms and show that they arise from network connectivity, whereas low-degree networks fragment and fail to sustain oscillations. Disrupting clustering self-similarity slightly reduces synchronization, but circadian rhythms remain robust, indicating that average degree, rather than clustering, is the dominant structural driver. These results highlight the resilience of SCN rhythms to network scaling and provide a framework for linking multi-scale network structure to biological timekeeping.

physics.soc-ph

Recovery of activation propagation and self-sustained oscillation abilities in stroke brain networks

Healthy brain networks usually show highly efficient information communication and self-sustained oscillation abilities. However, how the brain network structure affects these dynamics after an injury (stroke) is not very clear. The recovery of structure and dynamics of stroke brain networks over time is still not known precisely. Based on the analysis of a large number of strokes' brain network data, we show that stroke changes the network properties in connection weights, average degree, clustering, community, etc. Yet, they will recover gradually over time to some extent. We then adopt a simplified reaction-diffusion model to investigate stroke patients' activation propagation and self-sustained oscillation abilities. Our results reveal that the stroke slows the adoption time across different brain scales, indicating a weakened brain's activation propagation ability. In addition, we show that the lifetime of self-sustained oscillatory patterns at three months post-stroke patients' brains significantly departs from the healthy one. Finally, we examine the properties of core networks of self-sustained oscillatory patterns, in which the directed edges denote the main pathways of activation propagation. Our results demonstrate that the lifetime and recovery of self-sustaining patterns are related to the properties of core networks, and the properties in the post-stroke greatly vary from those in the healthy group. Most importantly, the strokes' activation propagation and self-sustained oscillation abilities significantly improve at one year post-stroke, driven by structural connection repair. This work may help us to understand the relationship between structure and function in brain disorders.

physics.soc-ph