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Previous studies have observed that electromagnetic induction can seriously affect the electrophysiological activity of the nervous system. Considering the role of astrocytes in regulating neural firing, we studied a simple neuron–astrocyte coupled system under electromagnetic induction in response to different types of external stimulation. Both the duration and intensity of the external stimulus can induce different modes of electrical activity in this system, and thus the neuronal firing patterns can be subtly controlled. When the external stimulation ceases, the neuron will continue to fire for a long time and then reset to its resting state. In this study, “delay” is defined as the delayed time from the firing state to the resting state, and it is highly sensitive to changes in the duration or intensity of the external stimulus. Meanwhile, the self-similarity embodied in the aforementioned sensitivity can be quantified by fractal dimension. Moreover, a hysteresis loop of calcium activity in the astrocyte is observed in the specific interval of the external stimulus when the stimulus duration is extended to infinity, since astrocytic calcium or neuron electrical activity in the resting state or during periodic oscillation depends on the initial state. Finally, the regulating effect of electromagnetic induction in this system is considered. It is clarified that the occurrence of “delay” depends purely on the existence of electromagnetic induction. This model can reveal the dynamic characteristics of the neuron–astrocyte coupling system with magnetic induction under external stimulation. These results can provide some insights into the effects of electromagnetic induction and stimulation on neuronal activity.

As a large group of cells in a central nervous system, astrocytes have a great influence on ion and energy metabolism in a nervous system. Disorders of neuronal ion and energy metabolism caused by impaired astrocytes play a key role in the pathogenesis of epilepsy. This paper reviews the existing computational models of epileptogenesis resulting from impaired astrocytes and presents several open perspectives with regard to ion and energy metabolism-induced epileptogenesis in a neuron-astrocyte-capillary coupled model.

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Astrocytes play a crucial role in neuronal firing activity. Their abnormal state may lead to the pathological transition of neuronal firing patterns and even induce seizures. However, there is still little evidence explaining how the astrocyte network modulates seizures caused by structural abnormalities, such as gliosis. To explore the role of gliosis of the astrocyte network in epileptic seizures, we first established a direct astrocyte feedback neuronal network model on the basis of the hippocampal CA3 neuron-astrocyte model to simulate the condition of gliosis when astrocyte processes swell and the feedback to neurons increases in an abnormal state. We analyzed the firing pattern transitions of the neuronal network when astrocyte feedback starts to change via increases in both astrocyte feedback intensity and the connection probability of astrocytes to neurons in the network. The results show that as the connection probability and astrocyte feedback intensity increase, neuronal firing transforms from a nonepileptic synchronous firing state to an asynchronous firing state, and when astrocyte feedback starts to become abnormal, seizure-like firing becomes more severe and synchronized; meanwhile, the synchronization area continues to expand and eventually transforms into long-term seizure-like synchronous firing. Therefore, our results prove that astrocyte feedback can regulate the firing of the neuronal network, and when the astrocyte network develops gliosis, there will be an increase in the induction rate of epileptic seizures.