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<p>This study investigates how electromagnetic induction and astrocytic modulation jointly influence firing dynamics and synchronization in excitatory-inhibitory neuronal networks. Using a computational model that integrates pyramidal neurons, interneurons, and astrocytes with memristor-based electromagnetic feedback and calcium-dependent signaling, we demonstrate that electromagnetic induction generally suppresses neuronal firing, but this effect can be bidirectionally modulated by astrocytic feedback depending on intracellular calcium levels. Key findings reveal the non-linear dependence of neuronal responses on astrocytic calcium thresholds and <InlineEquation ID="IEq1"> <EquationSource Format="TEX">\(r_{\mathrm {IP_3}}\)</EquationSource> </InlineEquation> dynamics; the distinct roles of excitatory, inhibitory, and astrocytic coupling in regulating network synchrony and chimera states; and the existence of parameter regimes where astrocytic feedback is overridden under strong electromagnetic induction. These results highlight the critical interplay between electromagnetic and glial mechanisms in shaping network activity, offering insights for models of neural synchronization and potential therapeutic strategies for epilepsy and related disorders.</p>

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Exploring electromagnetic induction and astrocyte influence in excitatory-inhibitory coupling neuron network

  • 期刊论文

  • 发表日期：

    2026年4月21日

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  • Zhongquan Gao,
  • Peihua Feng

摘要

This study investigates how electromagnetic induction and astrocytic modulation jointly influence firing dynamics and synchronization in excitatory-inhibitory neuronal networks. Using a computational model that integrates pyramidal neurons, interneurons, and astrocytes with memristor-based electromagnetic feedback and calcium-dependent signaling, we demonstrate that electromagnetic induction generally suppresses neuronal firing, but this effect can be bidirectionally modulated by astrocytic feedback depending on intracellular calcium levels. Key findings reveal the non-linear dependence of neuronal responses on astrocytic calcium thresholds and \(r_{\mathrm {IP_3}}\) dynamics; the distinct roles of excitatory, inhibitory, and astrocytic coupling in regulating network synchrony and chimera states; and the existence of parameter regimes where astrocytic feedback is overridden under strong electromagnetic induction. These results highlight the critical interplay between electromagnetic and glial mechanisms in shaping network activity, offering insights for models of neural synchronization and potential therapeutic strategies for epilepsy and related disorders.